Type 2 Diabetes ICYMI

Key clinical point: Sodium-glucose cotransporter-2 inhibitor (SGLT2i) vs dipeptidyl peptidase-4 inhibitor (DPP4i) use at discharge was associated with a lower risk for 1-year all-cause mortality and heart failure (HF) readmission in hospitalized patients with HF and type 2 diabetes (T2D) in a superaged society.

Major finding: Overall, 71.91% of patients were ≥75 years old. SGLT2i vs DPP4i significantly reduced the risk for 1-year all-cause mortality (adjusted hazard ratio [aHR] 0.70; 95% CI 0.56-0.89) and HF readmission (aHRk 0.52; 95% CI 0.45-0.61), with findings being similar among very elderly patients (age, ≥75 years).

Study details: Findings are from a retrospective study including patients hospitalized with the first episode of acute HF and T2D, of which 2101 patients with T2D receiving SGLT2i were propensity score-matched with 2101 of those receiving DPP4i.

Disclosures: This work was supported by Labor Research Grants from the Ministry of Health, Labour, and Welfare of Japan. The authors declared no conflicts of interest.

Source: Nakai M et al. Contemporary use of SGLT2 inhibitors in heart failure patients with diabetes mellitus: A comparison of DPP4 inhibitors in a nationwide electric health database of the superaged society. Cardiovasc Diabetol. 2022;21:157 (Aug 13). Doi: 10.1186/s12933-022-01586-6

Key clinical point: Sodium-glucose cotransporter-2 inhibitor (SGLT2i) vs dipeptidyl peptidase-4 inhibitor (DPP4i) use at discharge was associated with a lower risk for 1-year all-cause mortality and heart failure (HF) readmission in hospitalized patients with HF and type 2 diabetes (T2D) in a superaged society.

Major finding: Overall, 71.91% of patients were ≥75 years old. SGLT2i vs DPP4i significantly reduced the risk for 1-year all-cause mortality (adjusted hazard ratio [aHR] 0.70; 95% CI 0.56-0.89) and HF readmission (aHRk 0.52; 95% CI 0.45-0.61), with findings being similar among very elderly patients (age, ≥75 years).

Study details: Findings are from a retrospective study including patients hospitalized with the first episode of acute HF and T2D, of which 2101 patients with T2D receiving SGLT2i were propensity score-matched with 2101 of those receiving DPP4i.

Disclosures: This work was supported by Labor Research Grants from the Ministry of Health, Labour, and Welfare of Japan. The authors declared no conflicts of interest.

Source: Nakai M et al. Contemporary use of SGLT2 inhibitors in heart failure patients with diabetes mellitus: A comparison of DPP4 inhibitors in a nationwide electric health database of the superaged society. Cardiovasc Diabetol. 2022;21:157 (Aug 13). Doi: 10.1186/s12933-022-01586-6

Key clinical point: Sodium-glucose cotransporter-2 inhibitor (SGLT2i) vs dipeptidyl peptidase-4 inhibitor (DPP4i) use at discharge was associated with a lower risk for 1-year all-cause mortality and heart failure (HF) readmission in hospitalized patients with HF and type 2 diabetes (T2D) in a superaged society.

Major finding: Overall, 71.91% of patients were ≥75 years old. SGLT2i vs DPP4i significantly reduced the risk for 1-year all-cause mortality (adjusted hazard ratio [aHR] 0.70; 95% CI 0.56-0.89) and HF readmission (aHRk 0.52; 95% CI 0.45-0.61), with findings being similar among very elderly patients (age, ≥75 years).

Study details: Findings are from a retrospective study including patients hospitalized with the first episode of acute HF and T2D, of which 2101 patients with T2D receiving SGLT2i were propensity score-matched with 2101 of those receiving DPP4i.

Disclosures: This work was supported by Labor Research Grants from the Ministry of Health, Labour, and Welfare of Japan. The authors declared no conflicts of interest.

Source: Nakai M et al. Contemporary use of SGLT2 inhibitors in heart failure patients with diabetes mellitus: A comparison of DPP4 inhibitors in a nationwide electric health database of the superaged society. Cardiovasc Diabetol. 2022;21:157 (Aug 13). Doi: 10.1186/s12933-022-01586-6

Key clinical point: Dipeptidyl peptidase-4 (DPP4) inhibitors were more effective than other oral antidiabetic drugs (OAD) in reducing glycemic variability in patients with type 2 diabetes (T2D) receiving no concurrent insulin treatment.

Major finding: The mean amplitude of glycemic excursions reduced significantly in patients receiving DPP4 inhibitors vs other OAD (mean difference [MD] −0.69 mmol/L; P < .001), insulin secretagogues (MD −0.92 mmol/L; P < .001), non-secretagogues (MD −0.43 mmol/L; P = .02), sulfonylureas (MD −0.91 mmol/L; P < .001), and sodium-glucose cotransporter-2 inhibitors (MD −0.67 mmol/L; P = .03).

Study details: The data come from a meta-analysis of 14 randomized controlled trials including 855 patients with T2D.

Disclosures: This study was funded by MSD China Holding Co. Ltd. Four authors declared being employees of MSD China, and one author declared being an employee of Merck Sharp & Dohme LLC.

Source: Chai S et al. Influence of dipeptidyl peptidase-4 inhibitors on glycemic variability in patients with type 2 diabetes: A meta-analysis of randomized controlled trials. Front Endocrinol (Lausanne). 2022;13:935039 (Aug 9). Doi: 10.3389/fendo.2022.935039

Key clinical point: Dipeptidyl peptidase-4 (DPP4) inhibitors were more effective than other oral antidiabetic drugs (OAD) in reducing glycemic variability in patients with type 2 diabetes (T2D) receiving no concurrent insulin treatment.

Major finding: The mean amplitude of glycemic excursions reduced significantly in patients receiving DPP4 inhibitors vs other OAD (mean difference [MD] −0.69 mmol/L; P < .001), insulin secretagogues (MD −0.92 mmol/L; P < .001), non-secretagogues (MD −0.43 mmol/L; P = .02), sulfonylureas (MD −0.91 mmol/L; P < .001), and sodium-glucose cotransporter-2 inhibitors (MD −0.67 mmol/L; P = .03).

Study details: The data come from a meta-analysis of 14 randomized controlled trials including 855 patients with T2D.

Disclosures: This study was funded by MSD China Holding Co. Ltd. Four authors declared being employees of MSD China, and one author declared being an employee of Merck Sharp & Dohme LLC.

Source: Chai S et al. Influence of dipeptidyl peptidase-4 inhibitors on glycemic variability in patients with type 2 diabetes: A meta-analysis of randomized controlled trials. Front Endocrinol (Lausanne). 2022;13:935039 (Aug 9). Doi: 10.3389/fendo.2022.935039

Key clinical point: Dipeptidyl peptidase-4 (DPP4) inhibitors were more effective than other oral antidiabetic drugs (OAD) in reducing glycemic variability in patients with type 2 diabetes (T2D) receiving no concurrent insulin treatment.

Major finding: The mean amplitude of glycemic excursions reduced significantly in patients receiving DPP4 inhibitors vs other OAD (mean difference [MD] −0.69 mmol/L; P < .001), insulin secretagogues (MD −0.92 mmol/L; P < .001), non-secretagogues (MD −0.43 mmol/L; P = .02), sulfonylureas (MD −0.91 mmol/L; P < .001), and sodium-glucose cotransporter-2 inhibitors (MD −0.67 mmol/L; P = .03).

Study details: The data come from a meta-analysis of 14 randomized controlled trials including 855 patients with T2D.

Disclosures: This study was funded by MSD China Holding Co. Ltd. Four authors declared being employees of MSD China, and one author declared being an employee of Merck Sharp & Dohme LLC.

Source: Chai S et al. Influence of dipeptidyl peptidase-4 inhibitors on glycemic variability in patients with type 2 diabetes: A meta-analysis of randomized controlled trials. Front Endocrinol (Lausanne). 2022;13:935039 (Aug 9). Doi: 10.3389/fendo.2022.935039

Key clinical point: Sodium-glucose cotransporter-2 (SGLT-2) inhibitors did not have any significant beneficial effects on cardiac autonomic neuropathy (CAN) indices in patients with type 2 diabetes (T2D).

Major finding: SGLT-2 inhibitors had no significant effect on the low-frequency-to-high-frequency ratio (mean difference [MD] −0.11; P = .36), change in standard deviation of all 5-minute mean normal RR intervals (MD −2.83; P = .23), and change in the square root of the mean of the sum of the squares of differences between adjacent RR intervals (MD −0.14; P = .94).

Study details: Findings are from a meta-analysis of four randomized controlled trials including 247 patients with T2D who were randomly assigned to receive SGLT-2 inhibitors or placebo/active comparator.

Disclosures: This study did not receive any funding. The authors declared no conflicts of interest.

Source: Patoulias D et al. Effect of SGLT-2 inhibitors on cardiac autonomic function in type 2 diabetes mellitus: A meta-analysis of randomized controlled trials. Acta Diabetol. 2022 (Aug 19). Doi: 10.1007/s00592-022-01958-0

Key clinical point: Sodium-glucose cotransporter-2 (SGLT-2) inhibitors did not have any significant beneficial effects on cardiac autonomic neuropathy (CAN) indices in patients with type 2 diabetes (T2D).

Major finding: SGLT-2 inhibitors had no significant effect on the low-frequency-to-high-frequency ratio (mean difference [MD] −0.11; P = .36), change in standard deviation of all 5-minute mean normal RR intervals (MD −2.83; P = .23), and change in the square root of the mean of the sum of the squares of differences between adjacent RR intervals (MD −0.14; P = .94).

Study details: Findings are from a meta-analysis of four randomized controlled trials including 247 patients with T2D who were randomly assigned to receive SGLT-2 inhibitors or placebo/active comparator.

Disclosures: This study did not receive any funding. The authors declared no conflicts of interest.

Source: Patoulias D et al. Effect of SGLT-2 inhibitors on cardiac autonomic function in type 2 diabetes mellitus: A meta-analysis of randomized controlled trials. Acta Diabetol. 2022 (Aug 19). Doi: 10.1007/s00592-022-01958-0

Key clinical point: Sodium-glucose cotransporter-2 (SGLT-2) inhibitors did not have any significant beneficial effects on cardiac autonomic neuropathy (CAN) indices in patients with type 2 diabetes (T2D).

Major finding: SGLT-2 inhibitors had no significant effect on the low-frequency-to-high-frequency ratio (mean difference [MD] −0.11; P = .36), change in standard deviation of all 5-minute mean normal RR intervals (MD −2.83; P = .23), and change in the square root of the mean of the sum of the squares of differences between adjacent RR intervals (MD −0.14; P = .94).

Study details: Findings are from a meta-analysis of four randomized controlled trials including 247 patients with T2D who were randomly assigned to receive SGLT-2 inhibitors or placebo/active comparator.

Disclosures: This study did not receive any funding. The authors declared no conflicts of interest.

Source: Patoulias D et al. Effect of SGLT-2 inhibitors on cardiac autonomic function in type 2 diabetes mellitus: A meta-analysis of randomized controlled trials. Acta Diabetol. 2022 (Aug 19). Doi: 10.1007/s00592-022-01958-0

Key clinical point: In patients with type 2 diabetes (T2D) advancing from basal insulin (BI) therapy, a once-daily insulin glargine 100 U/mL and lixisenatide (iGlarLixi) injection regimen showed similar glycemic control to multiple injections with BI plus rapid-acting insulin (RAI), without weight gain.

Major finding: At 6 months, the mean reduction in glycated hemoglobin with iGlarLixi was noninferior to BI+RAI (mean difference [MD] 0.1%; 1-sided P = .0032), with weight gain being significantly lower with iGlarLixi vs BI+RAI (MD −0.8 kg; 2-sided P = .0069). The incidence of hypoglycemia was similar between the treatment groups.

Study details: Findings are from a retrospective study that used propensity score matching to evaluate therapy advancement with iGlarLixi (n = 814) or BI+RAI (n = 814) in patients with T2D on BI therapy.

Disclosures: This study was funded by Sanofi, Paris, France. Some authors declared receiving honoraria for speaking or consulting or research support or serving as advisory board members or speakers for various sources, including Sanofi. Three authors reported being employees of Sanofi.

Source: McCrimmon RJ et al. iGlarLixi versus basal plus rapid-acting insulin in adults with type 2 diabetes advancing from basal insulin therapy: The SoliSimplify real-world study. Diabetes Obes Metab. 2022 (Aug 19). Doi: 10.1111/dom.14844

Key clinical point: In patients with type 2 diabetes (T2D) advancing from basal insulin (BI) therapy, a once-daily insulin glargine 100 U/mL and lixisenatide (iGlarLixi) injection regimen showed similar glycemic control to multiple injections with BI plus rapid-acting insulin (RAI), without weight gain.

Major finding: At 6 months, the mean reduction in glycated hemoglobin with iGlarLixi was noninferior to BI+RAI (mean difference [MD] 0.1%; 1-sided P = .0032), with weight gain being significantly lower with iGlarLixi vs BI+RAI (MD −0.8 kg; 2-sided P = .0069). The incidence of hypoglycemia was similar between the treatment groups.

Study details: Findings are from a retrospective study that used propensity score matching to evaluate therapy advancement with iGlarLixi (n = 814) or BI+RAI (n = 814) in patients with T2D on BI therapy.

Disclosures: This study was funded by Sanofi, Paris, France. Some authors declared receiving honoraria for speaking or consulting or research support or serving as advisory board members or speakers for various sources, including Sanofi. Three authors reported being employees of Sanofi.

Source: McCrimmon RJ et al. iGlarLixi versus basal plus rapid-acting insulin in adults with type 2 diabetes advancing from basal insulin therapy: The SoliSimplify real-world study. Diabetes Obes Metab. 2022 (Aug 19). Doi: 10.1111/dom.14844

Key clinical point: In patients with type 2 diabetes (T2D) advancing from basal insulin (BI) therapy, a once-daily insulin glargine 100 U/mL and lixisenatide (iGlarLixi) injection regimen showed similar glycemic control to multiple injections with BI plus rapid-acting insulin (RAI), without weight gain.

Major finding: At 6 months, the mean reduction in glycated hemoglobin with iGlarLixi was noninferior to BI+RAI (mean difference [MD] 0.1%; 1-sided P = .0032), with weight gain being significantly lower with iGlarLixi vs BI+RAI (MD −0.8 kg; 2-sided P = .0069). The incidence of hypoglycemia was similar between the treatment groups.

Study details: Findings are from a retrospective study that used propensity score matching to evaluate therapy advancement with iGlarLixi (n = 814) or BI+RAI (n = 814) in patients with T2D on BI therapy.

Disclosures: This study was funded by Sanofi, Paris, France. Some authors declared receiving honoraria for speaking or consulting or research support or serving as advisory board members or speakers for various sources, including Sanofi. Three authors reported being employees of Sanofi.

Source: McCrimmon RJ et al. iGlarLixi versus basal plus rapid-acting insulin in adults with type 2 diabetes advancing from basal insulin therapy: The SoliSimplify real-world study. Diabetes Obes Metab. 2022 (Aug 19). Doi: 10.1111/dom.14844

Key clinical point: Dapagliflozin significantly reduced kidney function decline in patients with type 2 diabetes (T2D) and a high cardiovascular disease (CVD) risk across all Kidney Disease: Improving Global Outcomes (KDIGO) risk categories, including those with low baseline end-stage kidney disease (ESKD) risk

Major finding: Dapagliflozin vs placebo led to a significant reduction in kidney-specific composite outcome across all KDIGO risk categories (P_interaction = .97), including those with low baseline kidney disease risk (hazard ratio 0.54; P < .001), with the risk for estimated glomerular filtration rate (eGFR) reductions by ≥30%, ≥40%, ≥50%, and ≥57% being significantly lower with dapagliflozin vs placebo (all P < .05).

Study details: Findings are from a post hoc analysis of the DECLARE-TIMI 58 trial including 16,842 patients with T2D at high CVD risk and low (n = 10,958), moderate (n = 4243), high (n = 1403), and very high (n = 238) ESKD risk according to KDIGO risk categories.

Disclosures: The DECLARE-TIMI 58 trial was funded by AstraZeneca and Bristol-Myers Squibb. Some authors reported receiving research funding, grant support, honoraria, personal fees, or consultancy fees or serving as advisory board members for various resources.

Source: Mosenzon O et al. Dapagliflozin and prevention of kidney disease among patients with type 2 diabetes--Post hoc analyses from the DECLARE-TIMI 58 trial. Diabetes Care. 2022 (Aug 23). Doi: 10.2337/dc22-0382

Key clinical point: Dapagliflozin significantly reduced kidney function decline in patients with type 2 diabetes (T2D) and a high cardiovascular disease (CVD) risk across all Kidney Disease: Improving Global Outcomes (KDIGO) risk categories, including those with low baseline end-stage kidney disease (ESKD) risk

Major finding: Dapagliflozin vs placebo led to a significant reduction in kidney-specific composite outcome across all KDIGO risk categories (P_interaction = .97), including those with low baseline kidney disease risk (hazard ratio 0.54; P < .001), with the risk for estimated glomerular filtration rate (eGFR) reductions by ≥30%, ≥40%, ≥50%, and ≥57% being significantly lower with dapagliflozin vs placebo (all P < .05).

Study details: Findings are from a post hoc analysis of the DECLARE-TIMI 58 trial including 16,842 patients with T2D at high CVD risk and low (n = 10,958), moderate (n = 4243), high (n = 1403), and very high (n = 238) ESKD risk according to KDIGO risk categories.

Disclosures: The DECLARE-TIMI 58 trial was funded by AstraZeneca and Bristol-Myers Squibb. Some authors reported receiving research funding, grant support, honoraria, personal fees, or consultancy fees or serving as advisory board members for various resources.

Source: Mosenzon O et al. Dapagliflozin and prevention of kidney disease among patients with type 2 diabetes--Post hoc analyses from the DECLARE-TIMI 58 trial. Diabetes Care. 2022 (Aug 23). Doi: 10.2337/dc22-0382

Key clinical point: Dapagliflozin significantly reduced kidney function decline in patients with type 2 diabetes (T2D) and a high cardiovascular disease (CVD) risk across all Kidney Disease: Improving Global Outcomes (KDIGO) risk categories, including those with low baseline end-stage kidney disease (ESKD) risk

Major finding: Dapagliflozin vs placebo led to a significant reduction in kidney-specific composite outcome across all KDIGO risk categories (P_interaction = .97), including those with low baseline kidney disease risk (hazard ratio 0.54; P < .001), with the risk for estimated glomerular filtration rate (eGFR) reductions by ≥30%, ≥40%, ≥50%, and ≥57% being significantly lower with dapagliflozin vs placebo (all P < .05).

Study details: Findings are from a post hoc analysis of the DECLARE-TIMI 58 trial including 16,842 patients with T2D at high CVD risk and low (n = 10,958), moderate (n = 4243), high (n = 1403), and very high (n = 238) ESKD risk according to KDIGO risk categories.

Disclosures: The DECLARE-TIMI 58 trial was funded by AstraZeneca and Bristol-Myers Squibb. Some authors reported receiving research funding, grant support, honoraria, personal fees, or consultancy fees or serving as advisory board members for various resources.

Source: Mosenzon O et al. Dapagliflozin and prevention of kidney disease among patients with type 2 diabetes--Post hoc analyses from the DECLARE-TIMI 58 trial. Diabetes Care. 2022 (Aug 23). Doi: 10.2337/dc22-0382

Key clinical point: Patients with type 2 diabetes (T2D) and new-onset atrial fibrillation (AF) are at a higher risk for subsequent atherosclerotic cardiovascular disease (ASCVD), heart failure (HF), chronic kidney disease (CKD), all-cause mortality, and cardiovascular disease (CVD) mortality compared with those with T2D and without new-onset AF.

Major finding: Among patients with T2D, those with vs without incident AF had a higher risk for ASCVD (adjusted hazard ratio [aHR] 1.85; 95% CI 1.59-2.16), HF (aHR 4.40; 95% CI 3.67-5.28), CKD (aHR 1.68; 95% CI 1.41-2.01), all-cause mortality (aHR 2.91; 95% CI 2.53-3.34), and CVD mortality (aHR 3.75; 95% CI 2.93-4.80).

Study details: This study included 16,551 patients with T2D and without CVD and CKD, of which 1394 developed AF during follow-up.

Disclosures: This study did not receive any funding. No potential conflicts of interest were reported.

Source: Geng T et al. Associations of new-onset atrial fibrillation with risks of cardiovascular disease, chronic kidney disease, and mortality among patients with type 2 diabetes. Diabetes Care. 2022 (Aug 19). Doi: 10.2337/dc22-0717

Key clinical point: Patients with type 2 diabetes (T2D) and new-onset atrial fibrillation (AF) are at a higher risk for subsequent atherosclerotic cardiovascular disease (ASCVD), heart failure (HF), chronic kidney disease (CKD), all-cause mortality, and cardiovascular disease (CVD) mortality compared with those with T2D and without new-onset AF.

Major finding: Among patients with T2D, those with vs without incident AF had a higher risk for ASCVD (adjusted hazard ratio [aHR] 1.85; 95% CI 1.59-2.16), HF (aHR 4.40; 95% CI 3.67-5.28), CKD (aHR 1.68; 95% CI 1.41-2.01), all-cause mortality (aHR 2.91; 95% CI 2.53-3.34), and CVD mortality (aHR 3.75; 95% CI 2.93-4.80).

Study details: This study included 16,551 patients with T2D and without CVD and CKD, of which 1394 developed AF during follow-up.

Disclosures: This study did not receive any funding. No potential conflicts of interest were reported.

Source: Geng T et al. Associations of new-onset atrial fibrillation with risks of cardiovascular disease, chronic kidney disease, and mortality among patients with type 2 diabetes. Diabetes Care. 2022 (Aug 19). Doi: 10.2337/dc22-0717

Key clinical point: Patients with type 2 diabetes (T2D) and new-onset atrial fibrillation (AF) are at a higher risk for subsequent atherosclerotic cardiovascular disease (ASCVD), heart failure (HF), chronic kidney disease (CKD), all-cause mortality, and cardiovascular disease (CVD) mortality compared with those with T2D and without new-onset AF.

Major finding: Among patients with T2D, those with vs without incident AF had a higher risk for ASCVD (adjusted hazard ratio [aHR] 1.85; 95% CI 1.59-2.16), HF (aHR 4.40; 95% CI 3.67-5.28), CKD (aHR 1.68; 95% CI 1.41-2.01), all-cause mortality (aHR 2.91; 95% CI 2.53-3.34), and CVD mortality (aHR 3.75; 95% CI 2.93-4.80).

Study details: This study included 16,551 patients with T2D and without CVD and CKD, of which 1394 developed AF during follow-up.

Disclosures: This study did not receive any funding. No potential conflicts of interest were reported.

Source: Geng T et al. Associations of new-onset atrial fibrillation with risks of cardiovascular disease, chronic kidney disease, and mortality among patients with type 2 diabetes. Diabetes Care. 2022 (Aug 19). Doi: 10.2337/dc22-0717

Key clinical point: Canagliflozin reduced not only the risk for the first cardiovascular (CV) events but also subsequent CV events in patients with type 2 diabetes and chronic kidney disease (CKD), with absolute benefits being greater for total CV events.

Major finding: Canagliflozin reduced the risk for the first (hazard ratio 0.74; P < .001) and total (incidence rate ratio 0.71; P < .001) CV events by 26% and 29%, respectively, with the absolute risk difference per 1000 patients treated over 2.5 years being −44 (95% CI −67 to −21) and −73 (95% CI −114 to −33) for the first and total CV events, respectively.

Study details: This was a post hoc analysis of the CREDENCE trial including patients with type 2 diabetes (T2D; glycated hemoglobin 6.5%-12.0%) and CKD who were randomly assigned to receive canagliflozin or placebo.

Disclosures: The CREDENCE trial was sponsored by Janssen Research & Development, LLC. Some authors reported serving as advisory board members, speakers, or consultants, or receiving honoraria, research support, consulting, travel, or scientific presentation fees from various sources, including Janssen.

Source: Li JW et al. Effect of canagliflozin on total cardiovascular burden in patients with diabetes and chronic kidney disease: A post hoc analysis from the CREDENCE trial. J Am Heart Assoc. 2022;11(16):e025045 (Aug 5). Doi: 10.1161/JAHA.121.025045

Key clinical point: Canagliflozin reduced not only the risk for the first cardiovascular (CV) events but also subsequent CV events in patients with type 2 diabetes and chronic kidney disease (CKD), with absolute benefits being greater for total CV events.

Major finding: Canagliflozin reduced the risk for the first (hazard ratio 0.74; P < .001) and total (incidence rate ratio 0.71; P < .001) CV events by 26% and 29%, respectively, with the absolute risk difference per 1000 patients treated over 2.5 years being −44 (95% CI −67 to −21) and −73 (95% CI −114 to −33) for the first and total CV events, respectively.

Study details: This was a post hoc analysis of the CREDENCE trial including patients with type 2 diabetes (T2D; glycated hemoglobin 6.5%-12.0%) and CKD who were randomly assigned to receive canagliflozin or placebo.

Disclosures: The CREDENCE trial was sponsored by Janssen Research & Development, LLC. Some authors reported serving as advisory board members, speakers, or consultants, or receiving honoraria, research support, consulting, travel, or scientific presentation fees from various sources, including Janssen.

Source: Li JW et al. Effect of canagliflozin on total cardiovascular burden in patients with diabetes and chronic kidney disease: A post hoc analysis from the CREDENCE trial. J Am Heart Assoc. 2022;11(16):e025045 (Aug 5). Doi: 10.1161/JAHA.121.025045

Key clinical point: Canagliflozin reduced not only the risk for the first cardiovascular (CV) events but also subsequent CV events in patients with type 2 diabetes and chronic kidney disease (CKD), with absolute benefits being greater for total CV events.

Major finding: Canagliflozin reduced the risk for the first (hazard ratio 0.74; P < .001) and total (incidence rate ratio 0.71; P < .001) CV events by 26% and 29%, respectively, with the absolute risk difference per 1000 patients treated over 2.5 years being −44 (95% CI −67 to −21) and −73 (95% CI −114 to −33) for the first and total CV events, respectively.

Study details: This was a post hoc analysis of the CREDENCE trial including patients with type 2 diabetes (T2D; glycated hemoglobin 6.5%-12.0%) and CKD who were randomly assigned to receive canagliflozin or placebo.

Disclosures: The CREDENCE trial was sponsored by Janssen Research & Development, LLC. Some authors reported serving as advisory board members, speakers, or consultants, or receiving honoraria, research support, consulting, travel, or scientific presentation fees from various sources, including Janssen.

Source: Li JW et al. Effect of canagliflozin on total cardiovascular burden in patients with diabetes and chronic kidney disease: A post hoc analysis from the CREDENCE trial. J Am Heart Assoc. 2022;11(16):e025045 (Aug 5). Doi: 10.1161/JAHA.121.025045

Highlights of the European Association for the Study of Diabetes 2022 annual meeting include new data on weight loss with the blockbuster twincretin tirzepatide and on the effects of dapagliflozin on heart failure in people with diabetes, as well as updated guidelines for type 2 diabetes management.

The EASD meeting will take place Sept. 19-23 in Stockholm. It will be the first in-person meeting since 2019 but will also feature live-streamed content for participants around the world.

“The EASD congress will cover all the different areas and aspects of diabetes research – clinical, basic, epidemiologic, and psychological,” EASD President Stefano Del Prato, MD, told this news organization.

What attendees should expect, said Del Prato of the University of Pisa (Italy), “is the pleasure to be able to participate in person at a meeting and get useful information, not only in terms of the knowledge and intellectual aspects of diabetes, but also something that can be implemented the following day in their daily clinical activities.”  

EASD Honorary Secretary Mikael Rydén, MD, added: “I think meeting attendees will really be able to get the absolutely latest developments in all the areas that are relevant to diabetes treatments. It’s the best way to keep yourself up to date.”

This year, in particular, there’s a focus on past, present, and future trends in type 2 diabetes management, along with the co-occurring conditions of obesity, heart failure, and metabolic fatty liver disease.  
 

DELIVER: The diabetes side

On Sept. 22, new data will be presented from the DELIVER trial on the sodium-glucose cotransporter 2 (SGLT2) inhibitor dapagliflozin (Farxiga) in patients with heart failure with preserved ejection fraction, comparing data for participants with diabetes, prediabetes, and normoglycemia.

Primary results from DELIVER were presented Aug. 26 at the European Society of Cardiology Congress 2022 in Barcelona and simultaneously published in the New England Journal of Medicine. The results showed that dapagliflozin benefits patients with heart failure with preserved ejection fraction, as previously demonstrated in those with reduced ejection fraction in the DAPA-HF trial.

“This information is quite important and is becoming of major interest in the field of diabetes,” Dr. Del Prato said, adding that a related joint EASD/ESC symposium will take place the next morning, on Sept. 23, entitled, “New perspectives on heart function and failure in diabetes.”

“So, within the congress, you get the background, pathophysiology, the diagnostic aspects, and the results of the effect of dapagliflozin on those individuals.”

Dr. Rydén commented, “I think this underlines how important it is for diabetologists to screen our patients better for heart failure because we can actually treat them now.”

However, Dr. Rydén of the Karolinska Institute, Stockholm, also cautioned about use of SGLT2 inhibitors in people with diabetes who use insulin, given the risk of euglycemic diabetic ketoacidosis. “These drugs have side effects and you have to be wary who you prescribe them to. For those on multiple daily [insulin] injections, the side effects probably outweigh the benefits.”
 

Tirzepatide, weight loss, and type 2 diabetes remission

On Sept. 21, a symposium will provide new data for the dual glucagonlike peptide-1 (GLP-1) and glucose-dependent insulinotropic polypeptide (GIP) agonist tirzepatide, approved for the treatment of type 2 diabetes in the United States in May with the brand name Mounjaro. The agent is now being studied as an obesity treatment.

Data from the SURMOUNT-1 trial presented at the ADA meeting in June showed the drug produced “unprecedented” weight loss of up to 22.5%.

At EASD, those findings will be reviewed and new data presented on morbidity and mortality, along with a new commentary. The degree of weight loss seen with this new twincretin has furthered discussion about the concept of remission in type 2 diabetes, Dr. Rydén noted. That will also be the subject of the Diabetologia symposium on Sept. 21, entitled, “Remission of type 2 diabetes – fact or fiction?”

Regarding tirzepatide, Dr. Rydén said: “It’s amazing, the most powerful antiobesity drug we have at our disposal. These drugs slow gastric emptying and have other beneficial effects. … We’re now closing in on drugs that produce more than 15% weight loss. That appears to be the ‘magic bullet’ where you can achieve type 2 diabetes remission.” He pointed to a symposium sponsored by The Lancet on this topic at last year’s EASD meeting.

“I think what we want with our drugs is not to treat but actually to combat type 2 diabetes and really to achieve remission. Of course, if you’ve had it for many decades that might be impossible, but we know that particularly in the first 5-10 years it’s very important to have good glucose control and we know we can also achieve remission.”

Dr. Del Prato noted the importance of weight reduction at the time of type 2 diabetes diagnosis will be emphasized in the ADA/EASD consensus document on the management of hyperglycemia in type 2 diabetes, to be presented in its final form on Sept. 23.

“I think we’ll be learning more about potential remission in the future, both because of metabolic surgery and agents like tirzepatide. The reduction in body weight that can be achieved [with these newer drugs], or that has been reported so far, is the closest to what can be obtained with metabolic surgery. I think there will be more and more information and a lot of discussion about this, and of course about the definition of remission and what to do after remission has occurred,” Dr. Del Prato said.  

The revised ADA/EASD consensus document is expected to endorse weight loss as a “co-primary goal” of care for those without cardiorenal disease, along with early initiation of combination therapies – for example, taking two drugs immediately upon diagnosis, rather than just metformin – as opposed to the prior stepwise approach. The document will also cover use of newer glucose-lowering therapies, surgery, and behavioral interventions.  

The key is a holistic approach, Dr. Del Prato said. “Of course, glucose control is important, but it’s not the only thing. The heterogeneity of the population with diabetes is also important. Some may already have microvascular complications, kidney dysfunction, are more or less obese, and older or younger. We need to keep these differences in mind to provide more and more individualized treatment.”

Related to that, he noted, will be a joint EASD/ADA symposium on Sept. 19, entitled, “Precision medicine in type 2 diabetes: How far can we get?”
 

COVID-19 and diabetes, UKPDS, type 1 diabetes, and much more

As always, there’s a whole lot more. On Sept. 21, there will be a symposium on COVID-19 and diabetes.

Another, on diabetes technology, has a somewhat cautionary theme: “A new hope (Star Wars) or strange new worlds (Star Trek): Submerging diabetes into emerging technologies.” One of the speakers will address the question: “Are we becoming robots? Automated insulin delivery (AID) systems for everyone with type 1 diabetes: Strengths and limitations.” And this year’s EASD/JDRF symposium topic will be prevention of type 1 diabetes.

Yet another symposium on Sept. 21 will present 44-year follow-up data from the landmark United Kingdom Prospective Diabetes Study (UKPDS), including an economic analysis and a look at dementia outcomes. “It’s a historical thing. This big trial represents a gold mine of information,” Dr. Del Prato commented.

On Sept. 22, new data will be presented for the investigational once-weekly insulins during a symposium entitled, “Re-inventing the insulin experience: Exploring the prospects of once-weekly insulins.”

And lest anyone was thinking of leaving the conference early, there’s a full agenda on Sept. 23, including symposia on diabetic nephropathy, type 1 diabetes, diabetes in old age, dietary management, and the role of primary care, among others. There will also be 12 separate oral presentation sessions that day.

Overall, the meeting will reflect the multidisciplinary direction the field is headed, Dr. Rydén said.

“We’re still in an era of medicine where a lot of things happen every year. Now we have the next generation of drugs that are coming that combine many areas of treatment – obesity, cardiology, and nephrology. So, we’re integrating. The future is integrating the diabetes world with our friends in other areas of clinical medicine.”

Dr. Del Prato has reported being a consultant, advisory board member, and/or lecturer for AstraZeneca, Boehringer Ingelheim, Novo Nordisk, Sanofi, Takeda, Eli Lilly, Abbott, and Applied Therapeutics. Dr. Rydén has reported receiving lecture fees from the Novo Nordisk Foundation and serving on advisory boards for MSD, Lilly, Boehringer Ingelheim, and AstraZeneca.

A version of this article first appeared on Medscape.com.  
 

Highlights of the European Association for the Study of Diabetes 2022 annual meeting include new data on weight loss with the blockbuster twincretin tirzepatide and on the effects of dapagliflozin on heart failure in people with diabetes, as well as updated guidelines for type 2 diabetes management.

The EASD meeting will take place Sept. 19-23 in Stockholm. It will be the first in-person meeting since 2019 but will also feature live-streamed content for participants around the world.

“The EASD congress will cover all the different areas and aspects of diabetes research – clinical, basic, epidemiologic, and psychological,” EASD President Stefano Del Prato, MD, told this news organization.

What attendees should expect, said Del Prato of the University of Pisa (Italy), “is the pleasure to be able to participate in person at a meeting and get useful information, not only in terms of the knowledge and intellectual aspects of diabetes, but also something that can be implemented the following day in their daily clinical activities.”  

EASD Honorary Secretary Mikael Rydén, MD, added: “I think meeting attendees will really be able to get the absolutely latest developments in all the areas that are relevant to diabetes treatments. It’s the best way to keep yourself up to date.”

This year, in particular, there’s a focus on past, present, and future trends in type 2 diabetes management, along with the co-occurring conditions of obesity, heart failure, and metabolic fatty liver disease.  
 

DELIVER: The diabetes side

On Sept. 22, new data will be presented from the DELIVER trial on the sodium-glucose cotransporter 2 (SGLT2) inhibitor dapagliflozin (Farxiga) in patients with heart failure with preserved ejection fraction, comparing data for participants with diabetes, prediabetes, and normoglycemia.

Primary results from DELIVER were presented Aug. 26 at the European Society of Cardiology Congress 2022 in Barcelona and simultaneously published in the New England Journal of Medicine. The results showed that dapagliflozin benefits patients with heart failure with preserved ejection fraction, as previously demonstrated in those with reduced ejection fraction in the DAPA-HF trial.

“This information is quite important and is becoming of major interest in the field of diabetes,” Dr. Del Prato said, adding that a related joint EASD/ESC symposium will take place the next morning, on Sept. 23, entitled, “New perspectives on heart function and failure in diabetes.”

“So, within the congress, you get the background, pathophysiology, the diagnostic aspects, and the results of the effect of dapagliflozin on those individuals.”

Dr. Rydén commented, “I think this underlines how important it is for diabetologists to screen our patients better for heart failure because we can actually treat them now.”

However, Dr. Rydén of the Karolinska Institute, Stockholm, also cautioned about use of SGLT2 inhibitors in people with diabetes who use insulin, given the risk of euglycemic diabetic ketoacidosis. “These drugs have side effects and you have to be wary who you prescribe them to. For those on multiple daily [insulin] injections, the side effects probably outweigh the benefits.”
 

Tirzepatide, weight loss, and type 2 diabetes remission

On Sept. 21, a symposium will provide new data for the dual glucagonlike peptide-1 (GLP-1) and glucose-dependent insulinotropic polypeptide (GIP) agonist tirzepatide, approved for the treatment of type 2 diabetes in the United States in May with the brand name Mounjaro. The agent is now being studied as an obesity treatment.

Data from the SURMOUNT-1 trial presented at the ADA meeting in June showed the drug produced “unprecedented” weight loss of up to 22.5%.

At EASD, those findings will be reviewed and new data presented on morbidity and mortality, along with a new commentary. The degree of weight loss seen with this new twincretin has furthered discussion about the concept of remission in type 2 diabetes, Dr. Rydén noted. That will also be the subject of the Diabetologia symposium on Sept. 21, entitled, “Remission of type 2 diabetes – fact or fiction?”

Regarding tirzepatide, Dr. Rydén said: “It’s amazing, the most powerful antiobesity drug we have at our disposal. These drugs slow gastric emptying and have other beneficial effects. … We’re now closing in on drugs that produce more than 15% weight loss. That appears to be the ‘magic bullet’ where you can achieve type 2 diabetes remission.” He pointed to a symposium sponsored by The Lancet on this topic at last year’s EASD meeting.

“I think what we want with our drugs is not to treat but actually to combat type 2 diabetes and really to achieve remission. Of course, if you’ve had it for many decades that might be impossible, but we know that particularly in the first 5-10 years it’s very important to have good glucose control and we know we can also achieve remission.”

Dr. Del Prato noted the importance of weight reduction at the time of type 2 diabetes diagnosis will be emphasized in the ADA/EASD consensus document on the management of hyperglycemia in type 2 diabetes, to be presented in its final form on Sept. 23.

“I think we’ll be learning more about potential remission in the future, both because of metabolic surgery and agents like tirzepatide. The reduction in body weight that can be achieved [with these newer drugs], or that has been reported so far, is the closest to what can be obtained with metabolic surgery. I think there will be more and more information and a lot of discussion about this, and of course about the definition of remission and what to do after remission has occurred,” Dr. Del Prato said.  

The revised ADA/EASD consensus document is expected to endorse weight loss as a “co-primary goal” of care for those without cardiorenal disease, along with early initiation of combination therapies – for example, taking two drugs immediately upon diagnosis, rather than just metformin – as opposed to the prior stepwise approach. The document will also cover use of newer glucose-lowering therapies, surgery, and behavioral interventions.  

The key is a holistic approach, Dr. Del Prato said. “Of course, glucose control is important, but it’s not the only thing. The heterogeneity of the population with diabetes is also important. Some may already have microvascular complications, kidney dysfunction, are more or less obese, and older or younger. We need to keep these differences in mind to provide more and more individualized treatment.”

Related to that, he noted, will be a joint EASD/ADA symposium on Sept. 19, entitled, “Precision medicine in type 2 diabetes: How far can we get?”
 

COVID-19 and diabetes, UKPDS, type 1 diabetes, and much more

As always, there’s a whole lot more. On Sept. 21, there will be a symposium on COVID-19 and diabetes.

Another, on diabetes technology, has a somewhat cautionary theme: “A new hope (Star Wars) or strange new worlds (Star Trek): Submerging diabetes into emerging technologies.” One of the speakers will address the question: “Are we becoming robots? Automated insulin delivery (AID) systems for everyone with type 1 diabetes: Strengths and limitations.” And this year’s EASD/JDRF symposium topic will be prevention of type 1 diabetes.

Yet another symposium on Sept. 21 will present 44-year follow-up data from the landmark United Kingdom Prospective Diabetes Study (UKPDS), including an economic analysis and a look at dementia outcomes. “It’s a historical thing. This big trial represents a gold mine of information,” Dr. Del Prato commented.

On Sept. 22, new data will be presented for the investigational once-weekly insulins during a symposium entitled, “Re-inventing the insulin experience: Exploring the prospects of once-weekly insulins.”

And lest anyone was thinking of leaving the conference early, there’s a full agenda on Sept. 23, including symposia on diabetic nephropathy, type 1 diabetes, diabetes in old age, dietary management, and the role of primary care, among others. There will also be 12 separate oral presentation sessions that day.

Overall, the meeting will reflect the multidisciplinary direction the field is headed, Dr. Rydén said.

“We’re still in an era of medicine where a lot of things happen every year. Now we have the next generation of drugs that are coming that combine many areas of treatment – obesity, cardiology, and nephrology. So, we’re integrating. The future is integrating the diabetes world with our friends in other areas of clinical medicine.”

Dr. Del Prato has reported being a consultant, advisory board member, and/or lecturer for AstraZeneca, Boehringer Ingelheim, Novo Nordisk, Sanofi, Takeda, Eli Lilly, Abbott, and Applied Therapeutics. Dr. Rydén has reported receiving lecture fees from the Novo Nordisk Foundation and serving on advisory boards for MSD, Lilly, Boehringer Ingelheim, and AstraZeneca.

A version of this article first appeared on Medscape.com.  
 

Highlights of the European Association for the Study of Diabetes 2022 annual meeting include new data on weight loss with the blockbuster twincretin tirzepatide and on the effects of dapagliflozin on heart failure in people with diabetes, as well as updated guidelines for type 2 diabetes management.

The EASD meeting will take place Sept. 19-23 in Stockholm. It will be the first in-person meeting since 2019 but will also feature live-streamed content for participants around the world.

“The EASD congress will cover all the different areas and aspects of diabetes research – clinical, basic, epidemiologic, and psychological,” EASD President Stefano Del Prato, MD, told this news organization.

What attendees should expect, said Del Prato of the University of Pisa (Italy), “is the pleasure to be able to participate in person at a meeting and get useful information, not only in terms of the knowledge and intellectual aspects of diabetes, but also something that can be implemented the following day in their daily clinical activities.”  

EASD Honorary Secretary Mikael Rydén, MD, added: “I think meeting attendees will really be able to get the absolutely latest developments in all the areas that are relevant to diabetes treatments. It’s the best way to keep yourself up to date.”

This year, in particular, there’s a focus on past, present, and future trends in type 2 diabetes management, along with the co-occurring conditions of obesity, heart failure, and metabolic fatty liver disease.  
 

DELIVER: The diabetes side

On Sept. 22, new data will be presented from the DELIVER trial on the sodium-glucose cotransporter 2 (SGLT2) inhibitor dapagliflozin (Farxiga) in patients with heart failure with preserved ejection fraction, comparing data for participants with diabetes, prediabetes, and normoglycemia.

Primary results from DELIVER were presented Aug. 26 at the European Society of Cardiology Congress 2022 in Barcelona and simultaneously published in the New England Journal of Medicine. The results showed that dapagliflozin benefits patients with heart failure with preserved ejection fraction, as previously demonstrated in those with reduced ejection fraction in the DAPA-HF trial.

“This information is quite important and is becoming of major interest in the field of diabetes,” Dr. Del Prato said, adding that a related joint EASD/ESC symposium will take place the next morning, on Sept. 23, entitled, “New perspectives on heart function and failure in diabetes.”

“So, within the congress, you get the background, pathophysiology, the diagnostic aspects, and the results of the effect of dapagliflozin on those individuals.”

Dr. Rydén commented, “I think this underlines how important it is for diabetologists to screen our patients better for heart failure because we can actually treat them now.”

However, Dr. Rydén of the Karolinska Institute, Stockholm, also cautioned about use of SGLT2 inhibitors in people with diabetes who use insulin, given the risk of euglycemic diabetic ketoacidosis. “These drugs have side effects and you have to be wary who you prescribe them to. For those on multiple daily [insulin] injections, the side effects probably outweigh the benefits.”
 

Tirzepatide, weight loss, and type 2 diabetes remission

On Sept. 21, a symposium will provide new data for the dual glucagonlike peptide-1 (GLP-1) and glucose-dependent insulinotropic polypeptide (GIP) agonist tirzepatide, approved for the treatment of type 2 diabetes in the United States in May with the brand name Mounjaro. The agent is now being studied as an obesity treatment.

Data from the SURMOUNT-1 trial presented at the ADA meeting in June showed the drug produced “unprecedented” weight loss of up to 22.5%.

At EASD, those findings will be reviewed and new data presented on morbidity and mortality, along with a new commentary. The degree of weight loss seen with this new twincretin has furthered discussion about the concept of remission in type 2 diabetes, Dr. Rydén noted. That will also be the subject of the Diabetologia symposium on Sept. 21, entitled, “Remission of type 2 diabetes – fact or fiction?”

Regarding tirzepatide, Dr. Rydén said: “It’s amazing, the most powerful antiobesity drug we have at our disposal. These drugs slow gastric emptying and have other beneficial effects. … We’re now closing in on drugs that produce more than 15% weight loss. That appears to be the ‘magic bullet’ where you can achieve type 2 diabetes remission.” He pointed to a symposium sponsored by The Lancet on this topic at last year’s EASD meeting.

“I think what we want with our drugs is not to treat but actually to combat type 2 diabetes and really to achieve remission. Of course, if you’ve had it for many decades that might be impossible, but we know that particularly in the first 5-10 years it’s very important to have good glucose control and we know we can also achieve remission.”

Dr. Del Prato noted the importance of weight reduction at the time of type 2 diabetes diagnosis will be emphasized in the ADA/EASD consensus document on the management of hyperglycemia in type 2 diabetes, to be presented in its final form on Sept. 23.

“I think we’ll be learning more about potential remission in the future, both because of metabolic surgery and agents like tirzepatide. The reduction in body weight that can be achieved [with these newer drugs], or that has been reported so far, is the closest to what can be obtained with metabolic surgery. I think there will be more and more information and a lot of discussion about this, and of course about the definition of remission and what to do after remission has occurred,” Dr. Del Prato said.  

The revised ADA/EASD consensus document is expected to endorse weight loss as a “co-primary goal” of care for those without cardiorenal disease, along with early initiation of combination therapies – for example, taking two drugs immediately upon diagnosis, rather than just metformin – as opposed to the prior stepwise approach. The document will also cover use of newer glucose-lowering therapies, surgery, and behavioral interventions.  

The key is a holistic approach, Dr. Del Prato said. “Of course, glucose control is important, but it’s not the only thing. The heterogeneity of the population with diabetes is also important. Some may already have microvascular complications, kidney dysfunction, are more or less obese, and older or younger. We need to keep these differences in mind to provide more and more individualized treatment.”

Related to that, he noted, will be a joint EASD/ADA symposium on Sept. 19, entitled, “Precision medicine in type 2 diabetes: How far can we get?”
 

COVID-19 and diabetes, UKPDS, type 1 diabetes, and much more

As always, there’s a whole lot more. On Sept. 21, there will be a symposium on COVID-19 and diabetes.

Another, on diabetes technology, has a somewhat cautionary theme: “A new hope (Star Wars) or strange new worlds (Star Trek): Submerging diabetes into emerging technologies.” One of the speakers will address the question: “Are we becoming robots? Automated insulin delivery (AID) systems for everyone with type 1 diabetes: Strengths and limitations.” And this year’s EASD/JDRF symposium topic will be prevention of type 1 diabetes.

Yet another symposium on Sept. 21 will present 44-year follow-up data from the landmark United Kingdom Prospective Diabetes Study (UKPDS), including an economic analysis and a look at dementia outcomes. “It’s a historical thing. This big trial represents a gold mine of information,” Dr. Del Prato commented.

On Sept. 22, new data will be presented for the investigational once-weekly insulins during a symposium entitled, “Re-inventing the insulin experience: Exploring the prospects of once-weekly insulins.”

And lest anyone was thinking of leaving the conference early, there’s a full agenda on Sept. 23, including symposia on diabetic nephropathy, type 1 diabetes, diabetes in old age, dietary management, and the role of primary care, among others. There will also be 12 separate oral presentation sessions that day.

Overall, the meeting will reflect the multidisciplinary direction the field is headed, Dr. Rydén said.

“We’re still in an era of medicine where a lot of things happen every year. Now we have the next generation of drugs that are coming that combine many areas of treatment – obesity, cardiology, and nephrology. So, we’re integrating. The future is integrating the diabetes world with our friends in other areas of clinical medicine.”

Dr. Del Prato has reported being a consultant, advisory board member, and/or lecturer for AstraZeneca, Boehringer Ingelheim, Novo Nordisk, Sanofi, Takeda, Eli Lilly, Abbott, and Applied Therapeutics. Dr. Rydén has reported receiving lecture fees from the Novo Nordisk Foundation and serving on advisory boards for MSD, Lilly, Boehringer Ingelheim, and AstraZeneca.

A version of this article first appeared on Medscape.com.  
 

Chronic lack of exercise – dubbed “exercise deficiency” – is associated with cardiac atrophy, reduced cardiac output and chamber size, and diminished cardiorespiratory fitness (CRF) in a subgroup of patients with heart failure with preserved ejection fraction (HFpEF), researchers say.

Increasing the physical activity levels of these sedentary individuals could be an effective preventive strategy, particularly for those who are younger and middle-aged, they suggest.

Thinking of HFpEF as an exercise deficiency syndrome leading to a small heart “flies in the face of decades of cardiovascular teaching, because traditionally, we’ve thought of heart failure as the big floppy heart,” Andre La Gerche, MBBS, PhD, of the Baker Heart and Diabetes Institute, Melbourne, told this news organization.

“While it is true that some people with HFpEF have thick, stiff hearts, we propose that another subset has a normal heart, except it’s small because it’s been underexercised,” he said.

The article, published online  as part of a Focus Seminar series in the Journal of the American College of Cardiology, has “gone viral on social media,” Jason C. Kovacic, MBBS, PhD, of the Victor Chang Cardiac Research Institute, Darlinghurst, Australia, told this news organization.

Dr. Kovacic is a JACC section editor and the coordinating and senior author of the series, which covers other issues surrounding physical activity, both in athletes and the general public.
 

‘Coin-dropping moment’

To support their hypothesis that HFpEF is an exercise deficiency in certain patients, Dr. La Gerche and colleagues conducted a literature review that highlights the following points:

• There is a strong association between physical activity and both CRF and heart function.
• Exercise deficiency is a major risk factor for HFpEF in a subset of patients.
• Increasing physical activity is associated with greater cardiac mass, stroke volumes, cardiac output, and peak oxygen consumption.
• Physical inactivity leads to loss of heart muscle, reduced output and chamber size, and less ability to improve cardiac performance with exercise.
• Aging results in a smaller, stiffer heart; however, this effect is mitigated by regular exercise.
• Individuals who are sedentary throughout life cannot attenuate age-related reductions in heart size and have increasing chamber stiffness.

“When we explain it, it’s like a coin-dropping moment, because it’s actually a really simple concept,” Dr. La Gerche said. “A small heart has a small stroke volume. A patient with a small heart with a maximal stroke volume of 60 mL can generate a cardiac output of 9 L/min at a heart rate of 150 beats/min during exercise – an output that just isn’t enough. It’s like trying to drive a truck with a 50cc motorbike engine.”

“Plus,” Dr. La Gerche added, “exercise deficiency also sets the stage for comorbidities such as obesity, diabetes, and high blood pressure, all of which can ultimately lead to HFpEF.”

Considering HFpEF as an exercise deficiency syndrome has two clinical implications, Dr. La Gerche said. “First, it helps us understand the condition and diagnose more cases. For example, I think practitioners will start to recognize that breathlessness in some of their patients is associated with a small heart.”

“Second,” he said, “if it’s an exercise deficiency syndrome, the treatment is exercise. For most people, that means exercising regularly before the age of 60 to prevent HFpEF, because studies have found that after the age of 60, the heart is a bit fixed and harder to remodel. That doesn’t mean you shouldn’t try after 60 or that you won’t get benefit. But the real sweet spot is in middle age and younger.”
 

The bigger picture

The JACC Focus Seminar series starts with an article that underscores the benefits of regular physical activity. “The key is getting our patients to meet the guidelines: 150 to 300 minutes of moderate intensity exercise per week, or 75 to 250 minutes of vigorous activity per week,” Dr. Kovacic emphasized.

“Yes, we can give a statin to lower cholesterol. Yes, we can give a blood pressure medication to lower blood pressure. But when you prescribe exercise, you impact patients’ blood pressure, their cholesterol, their weight, their sense of well-being,” he said. “It cuts across so many different aspects of people’s lives that it’s important to underscore the value of exercise to everybody.”

That includes physicians, he affirmed. “It behooves all physicians to be leading by example. I would encourage those who are overweight or aren’t exercising as much as they should be to make the time to be healthy and to exercise. If you don’t, then bad health will force you to make the time to deal with bad health issues.”

Other articles in the series deal with the athlete’s heart. Christopher Semsarian, MBBS, PhD, MPH, University of Sydney, and colleagues discuss emerging data on hypertrophic cardiomyopathy and other genetic cardiovascular diseases, with the conclusion that it is probably okay for more athletes with these conditions to participate in recreational and competitive sports than was previously thought – another paradigm shift, according to Dr. Kovacic.

The final article addresses some of the challenges and controversies related to the athlete’s heart, including whether extreme exercise is associated with vulnerability to atrial fibrillation and other arrhythmias, and the impact of gender on the cardiac response to exercise, which can’t be determined now because of a paucity of data on women in sports.

Overall, Dr. Kovacic said, the series makes for “compelling” reading that should encourage readers to embark on their own studies to add to the data and support exercise prescription across the board.

No commercial funding or relevant conflicts of interest were reported.

A version of this article first appeared on Medscape.com.

Chronic lack of exercise – dubbed “exercise deficiency” – is associated with cardiac atrophy, reduced cardiac output and chamber size, and diminished cardiorespiratory fitness (CRF) in a subgroup of patients with heart failure with preserved ejection fraction (HFpEF), researchers say.

Increasing the physical activity levels of these sedentary individuals could be an effective preventive strategy, particularly for those who are younger and middle-aged, they suggest.

Thinking of HFpEF as an exercise deficiency syndrome leading to a small heart “flies in the face of decades of cardiovascular teaching, because traditionally, we’ve thought of heart failure as the big floppy heart,” Andre La Gerche, MBBS, PhD, of the Baker Heart and Diabetes Institute, Melbourne, told this news organization.

“While it is true that some people with HFpEF have thick, stiff hearts, we propose that another subset has a normal heart, except it’s small because it’s been underexercised,” he said.

The article, published online  as part of a Focus Seminar series in the Journal of the American College of Cardiology, has “gone viral on social media,” Jason C. Kovacic, MBBS, PhD, of the Victor Chang Cardiac Research Institute, Darlinghurst, Australia, told this news organization.

Dr. Kovacic is a JACC section editor and the coordinating and senior author of the series, which covers other issues surrounding physical activity, both in athletes and the general public.
 

‘Coin-dropping moment’

To support their hypothesis that HFpEF is an exercise deficiency in certain patients, Dr. La Gerche and colleagues conducted a literature review that highlights the following points:

• There is a strong association between physical activity and both CRF and heart function.
• Exercise deficiency is a major risk factor for HFpEF in a subset of patients.
• Increasing physical activity is associated with greater cardiac mass, stroke volumes, cardiac output, and peak oxygen consumption.
• Physical inactivity leads to loss of heart muscle, reduced output and chamber size, and less ability to improve cardiac performance with exercise.
• Aging results in a smaller, stiffer heart; however, this effect is mitigated by regular exercise.
• Individuals who are sedentary throughout life cannot attenuate age-related reductions in heart size and have increasing chamber stiffness.

“When we explain it, it’s like a coin-dropping moment, because it’s actually a really simple concept,” Dr. La Gerche said. “A small heart has a small stroke volume. A patient with a small heart with a maximal stroke volume of 60 mL can generate a cardiac output of 9 L/min at a heart rate of 150 beats/min during exercise – an output that just isn’t enough. It’s like trying to drive a truck with a 50cc motorbike engine.”

“Plus,” Dr. La Gerche added, “exercise deficiency also sets the stage for comorbidities such as obesity, diabetes, and high blood pressure, all of which can ultimately lead to HFpEF.”

Considering HFpEF as an exercise deficiency syndrome has two clinical implications, Dr. La Gerche said. “First, it helps us understand the condition and diagnose more cases. For example, I think practitioners will start to recognize that breathlessness in some of their patients is associated with a small heart.”

“Second,” he said, “if it’s an exercise deficiency syndrome, the treatment is exercise. For most people, that means exercising regularly before the age of 60 to prevent HFpEF, because studies have found that after the age of 60, the heart is a bit fixed and harder to remodel. That doesn’t mean you shouldn’t try after 60 or that you won’t get benefit. But the real sweet spot is in middle age and younger.”
 

The bigger picture

The JACC Focus Seminar series starts with an article that underscores the benefits of regular physical activity. “The key is getting our patients to meet the guidelines: 150 to 300 minutes of moderate intensity exercise per week, or 75 to 250 minutes of vigorous activity per week,” Dr. Kovacic emphasized.

“Yes, we can give a statin to lower cholesterol. Yes, we can give a blood pressure medication to lower blood pressure. But when you prescribe exercise, you impact patients’ blood pressure, their cholesterol, their weight, their sense of well-being,” he said. “It cuts across so many different aspects of people’s lives that it’s important to underscore the value of exercise to everybody.”

That includes physicians, he affirmed. “It behooves all physicians to be leading by example. I would encourage those who are overweight or aren’t exercising as much as they should be to make the time to be healthy and to exercise. If you don’t, then bad health will force you to make the time to deal with bad health issues.”

Other articles in the series deal with the athlete’s heart. Christopher Semsarian, MBBS, PhD, MPH, University of Sydney, and colleagues discuss emerging data on hypertrophic cardiomyopathy and other genetic cardiovascular diseases, with the conclusion that it is probably okay for more athletes with these conditions to participate in recreational and competitive sports than was previously thought – another paradigm shift, according to Dr. Kovacic.

The final article addresses some of the challenges and controversies related to the athlete’s heart, including whether extreme exercise is associated with vulnerability to atrial fibrillation and other arrhythmias, and the impact of gender on the cardiac response to exercise, which can’t be determined now because of a paucity of data on women in sports.

Overall, Dr. Kovacic said, the series makes for “compelling” reading that should encourage readers to embark on their own studies to add to the data and support exercise prescription across the board.

No commercial funding or relevant conflicts of interest were reported.

A version of this article first appeared on Medscape.com.

Chronic lack of exercise – dubbed “exercise deficiency” – is associated with cardiac atrophy, reduced cardiac output and chamber size, and diminished cardiorespiratory fitness (CRF) in a subgroup of patients with heart failure with preserved ejection fraction (HFpEF), researchers say.

Increasing the physical activity levels of these sedentary individuals could be an effective preventive strategy, particularly for those who are younger and middle-aged, they suggest.

Thinking of HFpEF as an exercise deficiency syndrome leading to a small heart “flies in the face of decades of cardiovascular teaching, because traditionally, we’ve thought of heart failure as the big floppy heart,” Andre La Gerche, MBBS, PhD, of the Baker Heart and Diabetes Institute, Melbourne, told this news organization.

“While it is true that some people with HFpEF have thick, stiff hearts, we propose that another subset has a normal heart, except it’s small because it’s been underexercised,” he said.

The article, published online  as part of a Focus Seminar series in the Journal of the American College of Cardiology, has “gone viral on social media,” Jason C. Kovacic, MBBS, PhD, of the Victor Chang Cardiac Research Institute, Darlinghurst, Australia, told this news organization.

Dr. Kovacic is a JACC section editor and the coordinating and senior author of the series, which covers other issues surrounding physical activity, both in athletes and the general public.
 

‘Coin-dropping moment’

To support their hypothesis that HFpEF is an exercise deficiency in certain patients, Dr. La Gerche and colleagues conducted a literature review that highlights the following points:

• There is a strong association between physical activity and both CRF and heart function.
• Exercise deficiency is a major risk factor for HFpEF in a subset of patients.
• Increasing physical activity is associated with greater cardiac mass, stroke volumes, cardiac output, and peak oxygen consumption.
• Physical inactivity leads to loss of heart muscle, reduced output and chamber size, and less ability to improve cardiac performance with exercise.
• Aging results in a smaller, stiffer heart; however, this effect is mitigated by regular exercise.
• Individuals who are sedentary throughout life cannot attenuate age-related reductions in heart size and have increasing chamber stiffness.

“When we explain it, it’s like a coin-dropping moment, because it’s actually a really simple concept,” Dr. La Gerche said. “A small heart has a small stroke volume. A patient with a small heart with a maximal stroke volume of 60 mL can generate a cardiac output of 9 L/min at a heart rate of 150 beats/min during exercise – an output that just isn’t enough. It’s like trying to drive a truck with a 50cc motorbike engine.”

“Plus,” Dr. La Gerche added, “exercise deficiency also sets the stage for comorbidities such as obesity, diabetes, and high blood pressure, all of which can ultimately lead to HFpEF.”

Considering HFpEF as an exercise deficiency syndrome has two clinical implications, Dr. La Gerche said. “First, it helps us understand the condition and diagnose more cases. For example, I think practitioners will start to recognize that breathlessness in some of their patients is associated with a small heart.”

“Second,” he said, “if it’s an exercise deficiency syndrome, the treatment is exercise. For most people, that means exercising regularly before the age of 60 to prevent HFpEF, because studies have found that after the age of 60, the heart is a bit fixed and harder to remodel. That doesn’t mean you shouldn’t try after 60 or that you won’t get benefit. But the real sweet spot is in middle age and younger.”
 

The bigger picture

The JACC Focus Seminar series starts with an article that underscores the benefits of regular physical activity. “The key is getting our patients to meet the guidelines: 150 to 300 minutes of moderate intensity exercise per week, or 75 to 250 minutes of vigorous activity per week,” Dr. Kovacic emphasized.

“Yes, we can give a statin to lower cholesterol. Yes, we can give a blood pressure medication to lower blood pressure. But when you prescribe exercise, you impact patients’ blood pressure, their cholesterol, their weight, their sense of well-being,” he said. “It cuts across so many different aspects of people’s lives that it’s important to underscore the value of exercise to everybody.”

That includes physicians, he affirmed. “It behooves all physicians to be leading by example. I would encourage those who are overweight or aren’t exercising as much as they should be to make the time to be healthy and to exercise. If you don’t, then bad health will force you to make the time to deal with bad health issues.”

Other articles in the series deal with the athlete’s heart. Christopher Semsarian, MBBS, PhD, MPH, University of Sydney, and colleagues discuss emerging data on hypertrophic cardiomyopathy and other genetic cardiovascular diseases, with the conclusion that it is probably okay for more athletes with these conditions to participate in recreational and competitive sports than was previously thought – another paradigm shift, according to Dr. Kovacic.

The final article addresses some of the challenges and controversies related to the athlete’s heart, including whether extreme exercise is associated with vulnerability to atrial fibrillation and other arrhythmias, and the impact of gender on the cardiac response to exercise, which can’t be determined now because of a paucity of data on women in sports.

Overall, Dr. Kovacic said, the series makes for “compelling” reading that should encourage readers to embark on their own studies to add to the data and support exercise prescription across the board.

No commercial funding or relevant conflicts of interest were reported.

A version of this article first appeared on Medscape.com.

Imagine that instead of a patient visiting their doctor for blood tests, they could rely on a noninvasive at-home test to predict their risk of diabetes, a disease that affects nearly 15% of U.S. adults (23% of whom are undiagnosed), according to the U.S. Centers for Disease Control and Prevention.

This technology could become a reality thanks to a research team that developed a machine learning algorithm to predict whether people had type 2 diabetes, prediabetes, or no diabetes. In an article published in BMJ Innovations, the researchers describe how their algorithm sorted people into these three categories with 97% accuracy on the basis of measurements of the heart’s electrical activity, determined from an electrocardiogram.

To develop and train their machine learning model – a type of artificial intelligence (AI) that keeps getting smarter over time – researchers used ECG measurements from 1,262 people in Central India. The study participants were part of the Sindhi population, an ethnic group that has been shown in past studies to be at elevated risk for type 2 diabetes.

Why ECG data? Because “cardiovascular abnormalities and diabetes, they go hand in hand,” says study author Manju Mamtani, MD, general manager of M&H Research, San Antonio, and treasurer of the Lata Medical Research Foundation. Subtle cardiovascular changes can occur even early in the development of diabetes.

“ECG has the power to detect these fluctuations, at least in theory, but those fluctuations are so tiny that many times we as humans looking at that might miss it,” says study author Hemant Kulkarni, MD, chief executive officer of M&H Research and president of the Lata Medical Research Foundation. “But the AI, which is powered to detect such specific fluctuations or subtle features, we hypothesized for the study that the AI algorithm might be able to pick those things up. And it did.”

Although this isn’t the first AI algorithm developed to predict diabetes risk, it outperforms previous models, the researchers say.

The team hopes to test and validate the algorithm in a variety of populations so that it can eventually be developed into an accessible, user-friendly technology. They envision that someday their algorithm could be used in smartwatches or other smart devices and could be integrated into telehealth so that people could be screened for diabetes even if they weren’t able to travel to a health care facility for blood testing.

The team is also studying other noninvasive methods of early disease detection and predictive models for adverse outcomes using AI.

“The fact that these algorithms are able to pick up the things of interest and learn on their own and keep learning in the future also adds excitement to their use in these settings,” says Dr. Kulkarni.

A version of this article first appeared on Medscape.com.

Imagine that instead of a patient visiting their doctor for blood tests, they could rely on a noninvasive at-home test to predict their risk of diabetes, a disease that affects nearly 15% of U.S. adults (23% of whom are undiagnosed), according to the U.S. Centers for Disease Control and Prevention.

This technology could become a reality thanks to a research team that developed a machine learning algorithm to predict whether people had type 2 diabetes, prediabetes, or no diabetes. In an article published in BMJ Innovations, the researchers describe how their algorithm sorted people into these three categories with 97% accuracy on the basis of measurements of the heart’s electrical activity, determined from an electrocardiogram.

To develop and train their machine learning model – a type of artificial intelligence (AI) that keeps getting smarter over time – researchers used ECG measurements from 1,262 people in Central India. The study participants were part of the Sindhi population, an ethnic group that has been shown in past studies to be at elevated risk for type 2 diabetes.

Why ECG data? Because “cardiovascular abnormalities and diabetes, they go hand in hand,” says study author Manju Mamtani, MD, general manager of M&H Research, San Antonio, and treasurer of the Lata Medical Research Foundation. Subtle cardiovascular changes can occur even early in the development of diabetes.

“ECG has the power to detect these fluctuations, at least in theory, but those fluctuations are so tiny that many times we as humans looking at that might miss it,” says study author Hemant Kulkarni, MD, chief executive officer of M&H Research and president of the Lata Medical Research Foundation. “But the AI, which is powered to detect such specific fluctuations or subtle features, we hypothesized for the study that the AI algorithm might be able to pick those things up. And it did.”

Although this isn’t the first AI algorithm developed to predict diabetes risk, it outperforms previous models, the researchers say.

The team hopes to test and validate the algorithm in a variety of populations so that it can eventually be developed into an accessible, user-friendly technology. They envision that someday their algorithm could be used in smartwatches or other smart devices and could be integrated into telehealth so that people could be screened for diabetes even if they weren’t able to travel to a health care facility for blood testing.

The team is also studying other noninvasive methods of early disease detection and predictive models for adverse outcomes using AI.

“The fact that these algorithms are able to pick up the things of interest and learn on their own and keep learning in the future also adds excitement to their use in these settings,” says Dr. Kulkarni.

A version of this article first appeared on Medscape.com.

Imagine that instead of a patient visiting their doctor for blood tests, they could rely on a noninvasive at-home test to predict their risk of diabetes, a disease that affects nearly 15% of U.S. adults (23% of whom are undiagnosed), according to the U.S. Centers for Disease Control and Prevention.

This technology could become a reality thanks to a research team that developed a machine learning algorithm to predict whether people had type 2 diabetes, prediabetes, or no diabetes. In an article published in BMJ Innovations, the researchers describe how their algorithm sorted people into these three categories with 97% accuracy on the basis of measurements of the heart’s electrical activity, determined from an electrocardiogram.

To develop and train their machine learning model – a type of artificial intelligence (AI) that keeps getting smarter over time – researchers used ECG measurements from 1,262 people in Central India. The study participants were part of the Sindhi population, an ethnic group that has been shown in past studies to be at elevated risk for type 2 diabetes.

Why ECG data? Because “cardiovascular abnormalities and diabetes, they go hand in hand,” says study author Manju Mamtani, MD, general manager of M&H Research, San Antonio, and treasurer of the Lata Medical Research Foundation. Subtle cardiovascular changes can occur even early in the development of diabetes.

“ECG has the power to detect these fluctuations, at least in theory, but those fluctuations are so tiny that many times we as humans looking at that might miss it,” says study author Hemant Kulkarni, MD, chief executive officer of M&H Research and president of the Lata Medical Research Foundation. “But the AI, which is powered to detect such specific fluctuations or subtle features, we hypothesized for the study that the AI algorithm might be able to pick those things up. And it did.”

Although this isn’t the first AI algorithm developed to predict diabetes risk, it outperforms previous models, the researchers say.

The team hopes to test and validate the algorithm in a variety of populations so that it can eventually be developed into an accessible, user-friendly technology. They envision that someday their algorithm could be used in smartwatches or other smart devices and could be integrated into telehealth so that people could be screened for diabetes even if they weren’t able to travel to a health care facility for blood testing.

The team is also studying other noninvasive methods of early disease detection and predictive models for adverse outcomes using AI.

“The fact that these algorithms are able to pick up the things of interest and learn on their own and keep learning in the future also adds excitement to their use in these settings,” says Dr. Kulkarni.

A version of this article first appeared on Medscape.com.