Sodium-glucose cotransporter type 2 inhibitors and cardiac arrhythmias

Manolis, Antonis A.; Manolis, Theodora A.; Melita, Helen; Manolis, Antonis S.

doi:10.1016/j.tcm.2022.04.003

Cited by 18 publications

(8 citation statements)

References 90 publications

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“…Previous reports hypothesized that SGLT2-I might induce changes in calcium ion currents, reducing calcium-related arrhythmogenesis. [ 42 – 44 ]. Another beneficial effect of SGLT2-I is the protection against hyperglycemia-induced sympathetic overstimulation slowing the action potential duration [ 45 ].…”

Section: Discussionmentioning

confidence: 99%

Outcomes in diabetic patients treated with SGLT2-Inhibitors with acute myocardial infarction undergoing PCI: The SGLT2-I AMI PROTECT Registry

Paolisso

Bergamaschi

Gragnano

et al. 2023

Pharmacological Research

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Section: Discussionmentioning

confidence: 99%

Outcomes in diabetic patients treated with SGLT2-Inhibitors with acute myocardial infarction undergoing PCI: The SGLT2-I AMI PROTECT Registry

Paolisso

Bergamaschi

Gragnano

et al. 2023

Pharmacological Research

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“…The relationship between SGLT2-i therapy and cardiac arrhythmias has been extensively studied in T2DM patients with HF, but reported results have been inconsistent ( 22 , 24 ). A systematic review and meta-analysis of randomized controlled trials on SGLT2i in T2DM patients highlighted that no significant difference was noted in the occurrence of AF in SGLT2-i patients ( 26 ).…”

Section: Discussionmentioning

confidence: 99%

“…Moreover, there seem to be no differences in protection from cardiac arrhythmias among different SGLT2-i, assuming a class effect ( 38 ). Less robust data regarding ventricular arrhythmias have been reported, possibly due to the large heterogeneity of the populations studied ( 22 , 24 ). Overall, there are encouraging data on reducing VAs in patients treated with SGLT2-i ( 35 , 39 ).…”

Section: Discussionmentioning

confidence: 99%

“…Patients with AMI, even those with T2DM, are prone to developing new-onset arrhythmias due to autonomic, electrical, and structural remodeling, and glycemic fluctuations ( 20 , 21 ). Although there is evidence for a reduction in new-onset arrhythmic events in patients treated with SGLT2-i, previous studies yielded inconclusive results and a variable association between SGLT2-i treatment and cardiac arrhythmias ( 22 – 24 ). Furthermore, the efficacy of SGLT2-i in preventing arrhythmic events in specific settings of diabetic patients with AMI remains unclear.…”

Section: Introductionmentioning

confidence: 99%

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In-hospital arrhythmic burden reduction in diabetic patients with acute myocardial infarction treated with SGLT2-inhibitors: Insights from the SGLT2-I AMI PROTECT study

Cesaro

Gragnano²,

Paolisso³

et al. 2022

Front. Cardiovasc. Med.

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BackgroundSodium-glucose co-transporter 2 inhibitors (SGLT2-i) have shown significant cardiovascular benefits in patients with and without type 2 diabetes mellitus (T2DM). They have also gained interest for their potential anti-arrhythmic role and their ability to reduce the occurrence of atrial fibrillation (AF) and ventricular arrhythmias (VAs) in T2DM and heart failure patients.ObjectivesTo investigate in-hospital new-onset cardiac arrhythmias in a cohort of T2DM patients presenting with acute myocardial infarction (AMI) treated with SGLT2-i vs. other oral anti-diabetic agents (non-SGLT2-i users).MethodsPatients from the SGLT2-I AMI PROTECT registry (NCT05261867) were stratified according to the use of SGLT2-i before admission for AMI, divided into SGLT2-i users vs. non-SGLT2-i users. In-hospital outcomes included the occurrence of in-hospital new-onset cardiac arrhythmias (NOCAs), defined as a composite of new-onset AF and sustained new-onset ventricular tachycardia (VT) and/or ventricular fibrillation (VF) during hospitalization.ResultsThe study population comprised 646 AMI patients categorized into SGLT2-i users (111 patients) and non-SGLT2-i users (535 patients). SGLT2-i users had a lower rate of NOCAs compared with non-SGLT2-i users (6.3 vs. 15.7%, p = 0.010). Moreover, SGLT2-i was associated with a lower rate of AF and VT/VF considered individually (p = 0.032). In the multivariate logistic regression model, after adjusting for all confounding factors, the use of SGLT2-i was identified as an independent predictor of the lower occurrence of NOCAs (OR = 0.35; 95%CI 0.14–0.86; p = 0.022). At multinomial logistic regression, after adjusting for potential confounders, SGLT2-i therapy remained an independent predictor of VT/VF occurrence (OR = 0.20; 95%CI 0.04–0.97; p = 0.046) but not of AF occurrence.ConclusionsIn T2DM patients, the use of SGLT2-i was associated with a lower risk of new-onset arrhythmic events during hospitalization for AMI. In particular, the primary effect was expressed in the reduction of VAs. These findings emphasize the cardioprotective effects of SGLT2-i in the setting of AMI beyond glycemic control.Trial registrationData are part of the observational international registry: SGLT2-I AMI PROTECT. ClinicalTrials.gov, identifier: NCT05261867.

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“…Sodium glucose cotransporter-2 (SGLT2) inhibitors or gliflozins improve HF-related outcomes and this beneficial influence occurs irrespective of the presence or absence of type 2 diabetes [9,[104][105][106][107]. The mechanisms accounting for these benefits are not well understood, but drug-induced osmotic diuresis and natriuresis seem to be the main contributing mechanisms, together with the preservation of glomerular filtration and facilitation of interstitial drainage, which can collectively translate into effective and safe decongestion [108].…”

Section: Sglt2 Inhibitorsmentioning

confidence: 99%

Neurohumoral Activation in Heart Failure

Manolis,

Manolis

2023

IJMS

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In patients with heart failure (HF), the neuroendocrine systems of the sympathetic nervous system (SNS), the renin–angiotensin–aldosterone system (RAAS) and the arginine vasopressin (AVP) system, are activated to various degrees producing often-observed tachycardia and concomitant increased systemic vascular resistance. Furthermore, sustained neurohormonal activation plays a key role in the progression of HF and may be responsible for the pathogenetic mechanisms leading to the perpetuation of the pathophysiology and worsening of the HF signs and symptoms. There are biomarkers of activation of these neurohormonal pathways, such as the natriuretic peptides, catecholamine levels and neprilysin and various newer ones, which may be employed to better understand the mechanisms of HF drugs and also aid in defining the subgroups of patients who might benefit from specific therapies, irrespective of the degree of left ventricular dysfunction. These therapies are directed against these neurohumoral systems (neurohumoral antagonists) and classically comprise beta blockers, angiotensin-converting enzyme (ACE) inhibitors/angiotensin receptor blockers and vaptans. Recently, the RAAS blockade has been refined by the introduction of the angiotensin receptor–neprilysin inhibitor (ARNI) sacubitril/valsartan, which combines the RAAS inhibition and neprilysin blocking, enhancing the actions of natriuretic peptides. All these issues relating to the neurohumoral activation in HF are herein reviewed, and the underlying mechanisms are pictorially illustrated.

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Sodium-glucose cotransporter type 2 inhibitors and cardiac arrhythmias

Cited by 18 publications

References 90 publications

Outcomes in diabetic patients treated with SGLT2-Inhibitors with acute myocardial infarction undergoing PCI: The SGLT2-I AMI PROTECT Registry

Outcomes in diabetic patients treated with SGLT2-Inhibitors with acute myocardial infarction undergoing PCI: The SGLT2-I AMI PROTECT Registry

In-hospital arrhythmic burden reduction in diabetic patients with acute myocardial infarction treated with SGLT2-inhibitors: Insights from the SGLT2-I AMI PROTECT study

Neurohumoral Activation in Heart Failure

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