Effects of sodium–glucose cotransporter-2 inhibitors on cardiac structural and electrical remodeling: from myocardial cytology to cardiodiabetology

2021 ◽  
Vol 20 ◽  
Author(s):  
Maria Marketou ◽  
Joanna Kontaraki ◽  
Spyros Maragkoudakis ◽  
Christos Danelatos ◽  
Sofia Papadaki ◽  
...  
Keyword(s):  
Ventricular Arrhythmias ◽  
Ventricular Hypertrophy ◽  
Myocardial Cell ◽  
Left Ventricular ◽  
Antiarrhythmic Action ◽  
Matrix Remodeling ◽  
Beneficial Effects ◽  
Concentric Hypertrophy ◽  
Sodium Glucose Cotransporter ◽  
Pleiotropic Actions

Abstract: Sodium-glucose cotransporter 2 inhibitors (SGLT2i) have changed the clinical landscape of diabetes mellitus (DM) therapy through their favourable effects on cardiovascular outcomes. Notably, the use of SGLT2i has been linked to cardiovascular benefits regardless of DM status, while their pleiotropic actions remain to be fully elucidated. What we do know is that SGLT2i exert beneficial effects even at the level of the myocardial cell, and that these are linked to an improvement in the energy substrate, resulting in less inflammation and fibrosis. SGLT2i ameliorate myocardial extracellular matrix remodeling, cardiomyocyte stiffness and concentric hypertrophy, achieving beneficial remodeling of the left ventricle with significant implications for the pathogenesis and outcome of heart failure. Most studies show a significant improvement in markers of diastolic dysfunction along with a reduction in left ventricular hypertrophy. In addition to these effects there is electrophysiological remodeling, which explains initial data suggesting that SGLT2i have an antiarrhythmic action against both atrial and ventricular arrhythmias. However, future studies need to clarify not only the exact mechanisms of this beneficial functional, structural, and electrophysiological cardiac remodeling, but also its magnitude, and to determine whether this is a class or a drug effect.

scholarly journals Is hypertensive left ventricular hypertrophy a cause of sustained ventricular arrhythmias in humans?

2021 ◽  
Author(s):  
R. Nadarajah ◽  
P. A. Patel ◽  
M. H. Tayebjee
Keyword(s):  
Left Ventricular Hypertrophy ◽  
Ventricular Arrhythmias ◽  
Ventricular Hypertrophy ◽  
Left Ventricular ◽  
Systemic Hypertension ◽  
Electrolyte Disturbance ◽  
Electrocardiographic Monitoring ◽  
Homogenous Distribution ◽  
Artery Disease ◽  
Asymptomatic Coronary Artery Disease

AbstractSudden cardiac death (SCD) is most commonly secondary to sustained ventricular arrhythmias (VAs). This review aimed to evaluate if left ventricular hypertrophy (LVH) secondary to systemic hypertension in humans is an isolated risk factor for ventricular arrhythmogenesis. Animal models of hypertensive LVH have shown changes in ion channel function and distribution, gap junction re-distribution and fibrotic deposition. Clinical data has consistently exhibited an increase in prevalence and complexity of non-sustained VAs on electrocardiographic monitoring. However, there is a dearth of trials suggesting progression to sustained VAs and SCD, with extrapolations being confounded by presence of co-existent asymptomatic coronary artery disease (CAD). Putatively, this lack of data may be due to the presence of more homogenous distribution of pathophysiological changes seen in those with hypertensive LVH versus known pro-arrhythmic conditions such as HCM and myocardial infarction. The overall impression is that sustained VAs in the context of hypertensive LVH are most likely to be precipitated by other causes such as CAD or electrolyte disturbance.

Risk of ventricular arrhythmias in left ventricular hypertrophy: The Framingham Heart Study

1987 ◽  
Vol 60 (7) ◽  
pp. 560-565 ◽  
Author(s):  
Daniel Levy ◽  
Keaven M. Anderson ◽  
Daniel D. Savage ◽  
Susan A. Balkus ◽  
William B. Kannel ◽  
...  
Keyword(s):  
Left Ventricular Hypertrophy ◽  
Framingham Heart Study ◽  
Ventricular Arrhythmias ◽  
Ventricular Hypertrophy ◽  
Left Ventricular ◽  
Heart Study

scholarly journals Serum Zinc and Selenium Concentrations in Patients with Hypertrophy and Remodelling of the Left Ventricle Secondary to Arterial Hypertension

Antioxidants ◽  
2021 ◽  
Vol 10 (11) ◽  
pp. 1803
Author(s):  
Paweł Gać ◽  
Karolina Czerwińska ◽  
Małgorzata Poręba ◽  
Adam Prokopowicz ◽  
Helena Martynowicz ◽  
...  
Keyword(s):  
Left Ventricle ◽  
Left Ventricular Hypertrophy ◽  
Arterial Hypertension ◽  
Ventricular Hypertrophy ◽  
Serum Zinc ◽  
Left Ventricular ◽  
Left Ventricular Geometry ◽  
Serum Selenium ◽  
Hypertensive Patients ◽  
Concentric Hypertrophy

The aim of the study was to assess the relationship between serum selenium and zinc concentrations (Se-S and Zn-S) and the left ventricle geometry in patients suffering from arterial hypertension. A total of 78 people with arterial hypertension (mean age: 53.72 ± 12.74 years) participated in the study. Se-S and Zn-S were determined in all patients. The type of left ventricular remodelling and hypertrophy was determined by the left ventricular mass index (LVMI) and relative wall thickness (RWT) measured by echocardiography. Se-S and Zn-S in the whole group were 89.84 ± 18.75 µg/L and 0.86 ± 0.13 mg/L. Normal left ventricular geometry was found in 28.2% of patients; left ventricular hypertrophy (LVH) in 71.8%, including concentric remodelling in 28.2%, concentric hypertrophy in 29.5%, and eccentric hypertrophy in 14.1%. LVH was statistically significantly more frequent in patients with Se-S < median compared to patients with Se-S ≥ median (87.2% vs. 56.4%, p < 0.05), as well as in patients with Zn-S < median compared to patients with Zn-S ≥ median (83.8% vs. 60.9%, p < 0.05). In hypertensive patients, older age, higher LDL cholesterol, higher fasting glucose, lower Se-S, and lower Zn-S were independently associated with LVH. In conclusion, in hypertensive patients, left ventricular hypertrophy may be associated with low levels of selenium and zinc in the serum.

scholarly journals Left ventricular hypertrophy in patients treated with regular hemodialyses

2008 ◽  
Vol 61 (7-8) ◽  
pp. 369-374 ◽  
Author(s):  
Dejan Petrovic ◽  
Biljana Stojimirovic
Keyword(s):  
Risk Factors ◽  
Left Ventricle ◽  
Left Ventricular Hypertrophy ◽  
Ventricular Hypertrophy ◽  
Pressure Overload ◽  
Left Ventricular ◽  
Cardiovascular Morbidity ◽  
Morbidity And Mortality ◽  
Concentric Hypertrophy ◽  
Cardiovascular Morbidity And Mortality

Left ventricular hypertrophy is the main risk factor for development of cardiovascular morbidity and mortality in patients on hemodialysis. Left ventricular hypertrophy is found in 75% of the patients treated with hemodialysis. Risk factors for left ventricular hypertrophy in patients on hemodialysis include: blood flow through arterial-venous fistula, anemia, hypertension, increased extracellular fluid volume, oxidative stress, microinflammation, hyperhomocysteinemia, secondary hyperpara- thyroidism, and disturbed calcium and phosphate homeostasis. Left ventricular pressure overload leads to parallel placement of new sarcomeres and development of concentric hypertrophy of left ventricle. Left ventricular hypertrophy advances in two stages. In the stage of adaptation, left ventricular hypertrophy occurs as a response to increased tension stress of the left ventricular wall and its action is protective. When volume and pressure overload the left ventricle chronically and without control, adaptive hypertrophy becomes maladaptive hypertrophy of the left ventricle, where myocytes are lost, systolic function is deranged and heart insufficiency is developed. Left ventricular mass index-LVMi greater than 131 g/m2 in men and greater than 100 g/m2 in women, and relative wall thickness of the left ventricle above 0.45 indicate concentric hypertrophy of the left ventricle. Eccentric hypertrophy of the left ventricle is defined echocardiographically as LVMi above 131 g/m2 in men and greater than 100 g/m2 in women, with RWT ?0.45. Identification of patients with increased risk for development of left ventricular hypertrophy and application of appropriate therapy to attain target values of risk factors lead to regression of left ventricular hypertrophy, reduced cardiovascular morbidity and mortality rates and improved quality of life in patients treated with regular hemodialyses.

scholarly journals Empagliflozin improves chronic hypercortisolism-induced abnormal myocardial structure and cardiac function in mice

2020 ◽  
Vol 11 ◽  
pp. 204062232097483
Author(s):  
Qing-Qing Zhang ◽  
Guo-Qing Li ◽  
Yi Zhong ◽  
Jie Wang ◽  
An-Ning Wang ◽  
...  
Keyword(s):  
Myocardial Dysfunction ◽  
Sglt2 Inhibitor ◽  
Heart Tissue ◽  
Left Ventricular ◽  
Tissue Samples ◽  
Beneficial Effects ◽  
Reduced Body ◽  
Sodium Glucose Cotransporter ◽  
And Function ◽  
Visceral Adipose

Background: Chronic exposure to excess glucocorticoids is frequently associated with a specific cardiomyopathy. Empagliflozin, a sodium-glucose cotransporter 2 (SGLT2) inhibitor, has beneficial effects as it aids in the reduction of heart failure and cardiovascular mortality in hospitalized patients. The aim of this study was to investigate the effects of empagliflozin on chronic hypercortisolism-induced myocardial fibrosis and myocardial dysfunction in mice. Methods: Male C57BL/6J mice (6 weeks old) were randomized to control, corticosterone (CORT), and empagliflozin + CORT groups. After 4 weeks of administration, heart structure and function were evaluated by echocardiography, and peripheral blood and tissue samples were collected. Expressions of Ccl2, Itgax, Mrc1, and Adgre1 mRNA in heart tissue were evaluated by RT-PCR, and signal transducer and activator of transcription 3 (STAT3) and Toll-like receptor 4 (TLR4) protein expression were analyzed by Western blotting. Results: Empagliflozin effectively reduced body weight, liver triglyceride, visceral adipose volume, and uric acid in CORT-treated mice. Left ventricular hypertrophy and cardiac dysfunction were improved significantly, phosphorylated STAT3 and TLR4 were alleviated, and macrophage infiltration in the myocardium was inhibited after administration of empagliflozin in CORT-treated mice. Conclusion: Empagliflozin has beneficial effects on specific cardiomyopathy associated with CORT, and the results provide new evidence that empagliflozin might be a potential drug for the prevention of this disease.

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