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How Diabetes Cause Heart Failure?

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How Diabetes Cause Heart Failure
How Diabetes Affects Your Heart – Over time, high blood sugar can damage blood vessels and the nerves that control your heart. People with diabetes are also more likely to have other conditions that raise the risk for heart disease:

High blood pressure increases the force of blood through your arteries and can damage artery walls. Having both high blood pressure and diabetes can greatly increase your risk for heart disease. Too much LDL (“bad”) cholesterol in your bloodstream can form plaque on damaged artery walls. High triglycerides (a type of fat in your blood) and low HDL (“good”) cholesterol or high LDL cholesterol is thought to contribute to hardening of the arteries.

None of these conditions has symptoms. Your doctor can check your blood pressure and do a simple blood test to see if your LDL, HDL, and triglyceride levels are high. These factors can also raise your risk for heart disease:

Smoking Being overweight or having obesity Not getting enough physical activity Eating a diet high in saturated fat, trans fat, cholesterol, and sodium (salt) Drinking too much alcohol

People with diabetes are also more likely to have heart failure, Heart failure is a serious condition, but it doesn’t mean the heart has stopped beating; it means your heart can’t pump blood well. This can lead to swelling in your legs and fluid building up in your lungs, making it hard to breathe. Get regular checkups to keep track of your heart health.

How does type 2 diabetes affect heart failure?

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Abstract Diabetes and heart failure are closely related: patients with diabetes have an increased risk of developing heart failure and those with heart failure are at higher risk of developing diabetes. Furthermore, antidiabetic medications increase the risk of mortality and hospitalisation for heart failure in patients with and without pre-existing heart failure. When the two diseases are considered individually, heart failure has a much poorer prognosis than diabetes mellitus; therefore heart failure has to be a priority for treatment in patients presenting with the two conditions, and the diabetic patient with heart failure should be managed by the heart failure team. No specific randomised clinical trials have been conducted to test the effect of cardiovascular drugs in diabetic patients with heart failure, but a wealth of evidence suggests that all interventions effective at improving prognosis in patients with heart failure are equally beneficial in patients with and without diabetes. The negative effect of glucose-lowering agents in patients with heart failure or at increased risk of heart failure has become evident after the withdrawal of rosiglitazone, a thiazolidinedione, from the EU market due to evidence of increased risk of cardiovascular events and hospitalisations for heart failure. An important issue that remains unresolved is the optimal target level of glycated haemoglobin, as recent studies have demonstrated significant reductions in total mortality, morbidity and risk of heart failure despite achieving HbA1c levels similar to those observed in the UKPDS study conducted some decades ago. Meta-analyses showed that intensive glucose lowering is not associated with any significant reduction in cardiovascular risk but conversely results in a significant increase in heart failure risk. Different medications have different risk: benefit ratios in diabetic patients with heart failure; therefore, the heart failure team must judge the required intensity of glycaemic control, the type and dose of glucose lowering agents and any change in glucose-lowering therapy, according to the clinical conditions present. Disclosure: The authors have no conflicts of interest to declare. Received: 28 September 2016 Accepted: 27 October 2016 Correspondence Details: Giuseppe MC Rosano, Clinical Academic Group Cardiovascular, St George’s Hospital NHS Trust Medical School, Cranmer Terrace, London, UK. E: [email protected] Copyright Statement: The copyright in this work belongs to Radcliffe Medical Media. Only articles clearly marked with the CC BY-NC logo are published with the Creative Commons by Attribution Licence. The CC BY-NC option was not available for Radcliffe journals before 1 January 2019. Articles marked ‘Open Access’ but not marked ‘CC BY-NC’ are made freely accessible at the time of publication but are subject to standard copyright law regarding reproduction and distribution. Permission is required for reuse of this content. Diabetes mellitus is highly prevalent amongst patients with heart failure, especially those with heart failure and preserved ejection fraction (HFpEF), and patients with the two conditions have a higher risk of mortality compared with patients without diabetes or heart failure.1–3 Diabetic patients have an increased risk of developing heart failure because of the abnormal cardiac handling of glucose and free fatty acids (FFAs), and because of the effect of the metabolic derangements of diabetes on the cardiovascular system. Furthermore, the metabolic risk of diabetes in heart failure is heightened by the effect of most anti-diabetic medications, as the use of certain anti-diabetic agents increase the risk of mortality and hospitalisation for heart failure both in patients with and without heart failure.4 This effect may be related to a direct effect of the glucose-lowering molecules on the cardiovascular system and/or to a negative effect of excessive glucose lowering, since lenient glycaemic control with newer therapeutic agents has shown to reduce significantly mortality, morbidity and risk of developing heart failure in diabeticpatients with proven cardiovascular disease.5 A wealth of epidemiological evidence demonstrates that diabetes mellitus is independently associated with the risk of developing heart failure, with the risk increasing by more than twofold in men and by more than fivefold in women.1-3,6 Heart failure is highly prevalent (25 % in chronic heart failure and up to 40 % in acute heart failure) in patients with diabetes mellitus. Its prevalence is four-times higher than that of the general population, suggesting a pathogenetic role of diabetes in heart failure. This pathogenetic role is also suggested by the fact that patients with diabetes and without heart failure have an increased risk of developing heart failure compared with a matched population (29 versus 18 %, respectively). In patients with diabetes mellitus, advanced age, duration of the disease, insulin use, presence of coronary artery disease and elevated serum creatinine are all independent risk factors for the development of heart failure.7 When the two diseases are considered individually, heart failure has a much poorer prognosis than diabetes mellitus, therefore heart failure has to be a priority for treatment in patients presenting with the two conditions, and the diabetic patient with heart failure should be managed by the heart failure team. This review will focus on the relationship between heart failure and type 2 diabetes mellitus. Mechanisms of Cardiac Dysfunction in Diabetes Mellitus The altered systemic and cardiac glucose metabolism of patients with the range of disease that go from impaired glucose control to diabetes mellitus contribute to the structural and functional abnormalities of the heart that culminate in cardiac dysfunction. In diabetic patients, heart failure develops not only because of the underlying coronary artery disease, but also because of the multiple pathophysiological and metabolic abnormalities induced by altered glucose metabolism.8 The impaired cardiac glucose metabolism and the switch of glucose to FFA oxidation that occurs in the diabetic heart has a significant negative effect on cardiac contractility and functioning thereby inducing left ventricular systolic and diastolic dysfunction even in the absence of coronary artery disease (CAD) or structured heart disease.9,10 The alteration of cardiac function in diabetics occurs through several different mechanisms, such as decreased glucose transport and carbohydrate oxidation, increase in FFA utilisation, decrease in sarcolemmal calcium transport, and alterations in myofibrillar regulatory contractile proteins. Cardiac glucose metabolism is compromised at several points in patients with diabetes mellitus: glucose uptake, glycolysis and intramitochondrial pyruvate oxidation. The reduction in the glucose uptake is due to the slow rate of glucose transport across the sarcolemmal membrane into the myocardium, secondary to a reduction in the myocardial concentration of glucose transporter type 1 (GLUT 1) and glucose transporter type 4 (GLUT 4). Patients with diabetes mellitus have higher plasma levels and myocardial uptake of FFA. High levels of circulating FFAs and their increased oxidation are primarily responsible for the inhibition of both glycolysis and glucose oxidation in the heart. Although the shift of cardiac energy substrate utilisation from glucose to FFA oxidation, occurring in the diabetic heart, is essential to ensure continuous adenosine triphosphate (ATP) generation to maintain heart function, this chronically maladaptation leads to decreased energetic reserves and cardiac efficiency. Indeed, diabetic hearts are characterised by a diminished production of high-energy phosphate, since the betaoxidation of FFA is less efficient than the glycolysis in generating energy (in relation to oxygen consumption) and may increase the risk of cardiac dysfunction during increased metabolic demands or ischaemia.9,10 Hyperglycaemia and insulin resistance also contribute to the development of heart failure through several different mechanisms acting independently and synergistically; such as impaired microvascular endothelial function, abnormal cardiac metabolism (shift myocardial utilisation of glucose toward less efficient fatty acid oxidation), increased myocardial fibrosis, increased oxidative stress and local activation of the renin-angiotensin system and sympathetic nervous system.9,10 Diabetes in Patients with Heart Failure Both population studies and clinical trials have demonstrated that diabetes mellitus significantly increases the risk of recurrent hospitalisations for heart failure and the duration of hospital stay in patients with heart failure, and it is associated with a significantly higher mortality compared with those without diabetes.11 In the Candesartan in Heart failure – Assessment of Reduction in Mortality and Morbidity (CHARM) programme the presence of diabetes mellitus was associated with a twofold increase of either death or the composite outcome of cardiovascular death or hospitalisation for heart failure in insulin users, and a 50 % increase risk in non-insulintreated diabetics.3 Diabetic patients with both reduced and preserved left ventricular ejection fraction show increased mortality and morbidity rates compared with patients without diabetes. This increased risk is also observed in those diabetic patients of either ischaemic or non-ischaemic origin. Of interest, the prognostic importance of diabetes mellitus becomes weaker in hospitalised patients for acute heart failure; suggesting that in these patients the prognosis depends more on the severity of cardiac decompensation rather than on metabolic abnormalities. The Treatment of Heart Failure in Diabetics No randomised clinical trials have been conducted to test the effect of cardiovascular interventions (drugs and/or devices) in diabetic patients with heart failure. However, abundant evidence suggests that all interventions effective at improving prognosis in patients with heart failure are equally beneficial in patients with and without diabetes.12 Beta-blockers and angiotensin-converting enzyme inhibitors are beneficial in patients with diabetes mellitus and their use is associated with reduced mortality and hospitalisations. Angiotensin II receptor blockers have shown similar efficacy in heart failure patients with and without diabetes. Although non-selective beta-blockers may have a negative effect on glycaemic control and increase the risk of future diabetes, and these effects may be less frequent with the more selective agents like bisoprolol, carvedilol and nebivolol, there is no reason to suggest a preferential use of a beta-blocker over another on the basis of the possible negative effect on glucose control. Despite a clear benefit of beta-blockers in heart failure patients with diabetes, these patients are still less likely to be discharged from hospital on a beta-blocker than non-diabetic patients with heart failure.12 Mineralocorticoid receptor antagonists are equally effective in patients with heart failure with and without diabetes mellitus. However, because of the frequent coexistence of diabetic nephropathy, a close surveillance of electrolyte and renal function is recommended in order to exclude hyperkalaemia. The two most recent drugs introduced in heart failure treatment, LCZ696 and ivabradine, are similarly effective in heart failure patients with and without diabetes, and should be implemented as suggested by the guidelines of the European Society of Cardiology/Heart Failure Association.12 Anti-diabetic Treatment in Patients with Diabetes and Heart Failure Glucose-lowering agents are known to increase the risk of cardiovascular events especially when a tight glycaemic control is pursued. Although initially linked to ischaemic heart disease, the negative effect of glucose-lowering agents in patients with heart failure or at increased risk of heart failure has become evident after rosiglitazone, a thiazolidinedione, was withdrawn from the EU market because of the evidence of increased risk of cardiovascular events.13 Despite the focus being mainly put on the risk of coronary events, it was evident even from the rosiglitazone saga that the most significant risk with the use of this drug(s) was related to heart failure. Glucose-lowering agents may favour the development of heart failure through several pathophysiological mechanisms related to the increased insulin levels, water retention and low glucose availability for the heart and muscles. The potential detrimental effect of the glucose lowering drugs cannot be dissected by the negative effect of excessive glucose lowering in diabetics. After the United Kingdom Prospective Diabetes Study (UKPDS) the majority of studies in diabetic patients aimed at glycated haemoglobin 1c (HbA1c) <7.5 % or even <7 %, and invariably reported an increased risk of cardiovascular events most often related to heart failure.1,14–18 Therefore, an important issue that is still unsolved is the target level of glycated haemoglobin that should be regarded as optimal – the recent Empagliflozin Cardiovascular Outcome Event Trial in Type 2 Diabetes Mellitus Patients (EMPA-REG) showed a significant reduction in total mortality, morbidity and risk of heart failure despite the achieved HbA1c which was 7.8 %.5 A meta-analysis of 13 studies including 34,533 patients showed that intensive glucose lowering is not associated with any significant reduction in cardiovascular risk but conversely results in a 47 % increase in risk of heart failure (P<0.001).19 A study conducted in a large cohort of heart failure patients with diabetes mellitus showed a U-shaped relationship between HbA1c and mortality, with the lowest risk in patients with moderate glycaemic control (HbA1c 7.1–8.0 %).14 These results are in agreement with the findings of the Action to Control Cardiovascular Risk in Diabetes (ACCORD) study, which demonstrated an increase of 21 % in the risk of death from all causes and of 35 % in the occurrence of cardiovascular death with tight control of glucose in patients with diabetes mellitus.20 The importance of hypoglycaemia has also been highlighted by the Eplerenone Post-Acute Myocardial Infarction Heart Failure Efficacy and Survival Study (EPHESUS) that found a 38 % increased risk of a poorer outcome among patients with hypoglycaemia complicating heart failure post-myocardial infarction (MI).21 The glucose-lowering treatment should be carefully evaluated and gradually implemented in diabetic patients with heart failure. Preference in the treatment of diabetic patients with heart failure should be given to metformin and empagliflozin that have shown to be safe and effective.5,22,23 Metformin is excreted though the kidney, therefore caution should be exerted in patients with impaired renal function and its use is contraindicated only in patients with severe renal or hepatic impairment. Sulphonylureas may frequently cause hypoglycaemia, although this risk is minimised by the slow release formulations. An increased risk of worsening heart failure has been reported with sulphanylureas in cohort studies including diabetic patients but has never been reported by randomised clinical trials.4 These drugs should be used with caution in diabetic patients with heart failure.12 Mitiglinides may induce water retention and should be used with caution in patients with heart failure. Alpha-glucosidase inhibitors like acarbose lack any effect on insulin, water and sodium retention, and are safe to use in patients with increased cardiovascular risk and in those with heart failure. Thiazolidinediones are associated with increased sodium and fluid retention, and increase sympathetic nervous system activity. Randomised clinical trials and meta-analyses have shown that thiazolidinediones increase the risk of heart failure worsening and hospitalisations from heart failure, and they are contraindicated in patients with heart failure.13 Dipeptidyl peptidase-4 inhibitors (DPP4is; gliptins) are trendy drugs for the control of glycaemia in patients with diabetes despite their small effect on HbA1c. Large randomised studies with DPP4i have cast doubts about their safety in heart failure showing an increased risk of heart failure hospitalisations, and despite recent data, suggest that they may be safe to use; given their limited clinical benefit and given that there is a lack of data on their effect in patients with heart failure their use is not recommended except under strict cardiology supervision.24,25,12,26 There are no data on the long term safety of glucagon-like peptide-1 (GLP-1) receptor agonists in patients with heart failure. Recently, liraglutide was tested against placebo in the Liraglutide Effect and Action in Diabetes: Evaluation of Cardiovascular Outcome Results (LEADER) trial and showed a significant reduction in the composite primary outcome of the first occurrence of cardiovascular death, nonfatal MI or non-fatal stroke, but no effect on heart failure endpoints. Given the absence of detailed data in patients with heart failure, the use of GLP-1 receptor agonists should be implemented only under strict cardiology supervision. The sodium-glucose cotransporter 2 inhibitors (SGLT2i) enhance glucose control by increasing the urinary excretion of glucose. Recently, the SGLT2i empagliflozin showed a significant and relevant effect on cardiovascular protection.5 The EMPA-REG OUTCOME study conducted in 7,020 patients with type 2 diabetes (glycated haemoglobin level, 7.0–10.0 %) at high risk for cardiovascular events followed for a median of 3.1 years has shown that empagliflozin use led to a significant reduction in the rates of death from cardiovascular causes (38 % relative risk reduction), hospitalisation for heart failure (35 % relative risk reduction) and death from any cause (32 % relative reduction). Empagliflozin reduced by 39 % the hospitalisations for or death from heart failure (2.8 versus 4.5 %; HR 0.61 ; P<0.001) and was associated with a reduction in all-cause hospitalisation (36.8 versus 39.6 %; HR 0.89 ; P=0.003). The mechanisms responsible for the effects of empagliflozin on cardiovascular endpoints and heart failure are largely unknown. Potential mechanisms to be proven include effect on sodium retention and plasma volume, osmotic diuresis, reduction of insulin levels and insulin response to food intake, modulation of the renin-angiotensin aldosterone system, reduction weight and blood pressure without increases in sympathetic nervous activity. Insulin is often required for the glucose control of diabetic patients with type 1 diabetes, and of some patients with type 2 diabetes and pancreatic islet beta cell exhaustion. Since insulin induces significant sodium retention precipitating worsening of heart failure, the change in dose, schedule of administration and type of insulin used must be constantly supervised by a cardiologist in patients with chronic heart failure. Therefore, the heart failure team according to the clinical conditions should make the judgement on the intensity of glycaemic control, the type and dose of glucose-lowering agents, and any change in the glucose-lowering therapy should be closely monitored. References

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  1. Stratton IM, Adler AI, Neil HA, et al. Association of glycaemia with macrovascular and microvascular complications of type 2 diabetes (UKPDS 35): prospective observational study. BMJ 2000; 321 :405–12. Crossref | PubMed
  2. Metra M, Zacà V, Parati G, et al. Cardiovascular and noncardiovascular comorbidities in patients with chronic heart failure. J Cardiovasc Med (Hagerstown) 2011; 12 :76–84. Crossref | PubMed
  3. MacDonald MR, Petrie MC, Varyani F, et al. Impact of diabetes on outcomes in patients with low and preserved ejection fraction heart failure: an analysis of the Candesartan in Heart failure: Assessment of Reduction in Mortality and morbidity (CHARM) programme. Eur Heart J 2008; 29 :1377–85. Crossref | PubMed
  4. Fadini GP, Avogaro A, Degli Esposti L, et al. Risk of hospitalization for heart failure in patients with type 2 diabetes newly treated with DPP-4 inhibitors or other oral glucose-lowering medications: a retrospective registry study on 127,555 patients from the Nationwide OsMed Health-DB Database. Eur Heart J 2015; 36 :2454–62. Crossref | PubMed
  5. Zinman B, Wanner C, Lachin JM, et al. Empagliflozin, cardiovascular outcomes, and mortality in type 2 diabetes. N Engl J Med 2015; 373 :2117–28. Crossref | PubMed
  6. Ryden L, Grant PJ, Anker SD, et al. ESC Guidelines on diabetes, pre-diabetes, and cardiovascular diseases developed in collaboration with the EASD: the Task Force on diabetes,pre-diabetes, and cardiovascular diseases of the European Society of Cardiology (ESC) and developed in collaboration with the EuropeanAssociation for the Study of Diabetes (EASD). Eur Heart J 2013; 34 :3035–87. Crossref | PubMed
  7. Wang Y, Negishi T, Negishi K, Marwick TH. Prediction of heart failure in patients with type 2 diabetes mellitus- a systematic review and meta-analysis. Diabetes Res Clin Pract 2015; 108 : 55–66. Crossref | PubMed
  8. Rosano GM, Vitale C, Fragasso G. Metabolic therapy for patients with diabetes mellitus and coronary artery disease. Am J Cardiol 2006; 98 (5A):14J–18J. Epub ahead of press. Crossref | PubMed
  9. Nagoshi T, Yoshimura M, Rosano GM, et al. Optimization of cardiac metabolism in heart failure. Curr Pharm Des 2011; 17 (35):3846–53. PMCID:PMC3271354 Crossref | PubMed
  10. Rosano GM, Fini M, Caminiti G, Barbaro G. Cardiac metabolism in myocardial ischemia. Curr Pharm Des 2008; 14 :2551–62. Crossref | PubMed
  11. Effect of enalapril on survival in patients with reduced left ventricular ejection fractions and congestive heart failure. The SOLVD Investigators. N Engl J Med 1991; 325 :293–302. Crossref | PubMed
  12. Ponikowski P, Voors A, Anker S, et al.2016 ESC Guidelines for the diagnosis and treatment of acute and chronic heart failure. The Task Force for the diagnosis and treatment of acute and chronic heart failure of the European Society of Cardiology (ESC). Eur J Heart Fail 2016; 37 :2129–200. Crossref | PubMed
  13. Home PD, Pocock SJ, Beck-Nielsen H, et al. Rosiglitazone evaluated for cardiovascular outcomes in oral agent combination therapy for type 2 diabetes (RECORD): a multicentre, randomised, open-label trial. Lancet 2009; 373 :2125–35. Crossref | PubMed
  14. Elder DH, Singh JS, Levin D, et al. Mean HbA1c and mortality in diabetic individuals with heart failure: a population cohort study. Eur J Heart Fail 2016; 18 :94–102. Crossref | PubMed
  15. Goode KM, John J, Rigby AS, et al. Elevated glycated haemoglobin is a strong predictor of mortality in patients with left ventricular systolic dysfunction who are not receiving treatment for diabetes mellitus. Heart 2009; 95 : 917–23. Crossref | PubMed
  16. Aguilar D, Bozkurt B, Ramasubbu K, Deswal A. Relationship of haemoglobin A1C and mortality in heart failure patients with diabetes. J Am Coll Cardiol 2009; 54 :422–8. PMCID:PMC2753214 Crossref | PubMed
  17. Jeffcoate SL. Diabetes control and complications: the role of glycated haemoglobin, 25 years on. Diabet Med 2004; 21 :657–65. Crossref | PubMed
  18. Lind M, Odén A, Fahlén M, Eliasson B. A systematic review of HbA1c variables used in the study of diabetic complications. Diabetes Metab Synd: Clin Res Rev 2008; 2 :282–93. Crossref
  19. Boussageon R, Bejan-Angoulvant T, Saadatian-Elahi M, et al. Effect of intensive glucose lowering treatment on all cause mortality, cardiovascular death, and microvascular events in type 2 diabetes: meta-analysis of randomised controlled trials. BMJ 2011; 343 :d4169. PMCID:PMC3144314; Crossref | PubMed
  20. ACCORD Study Group, Gerstein HC, Miller ME, Genuth S, et al. Long-term effects of intensive glucose lowering on cardiovascular outcomes. N Engl J Med 2011; 364 :818–28. PMCID:PMC4083508 Crossref | PubMed
  21. Ukena C, Dobre D, Mahfoud F, et al. Hypo- and hyperglycemia predict outcome in patients with left ventricular dysfunction after acute myocardial infarction: data from EPHESUS. J Card Fail 2012; 18 : 439–45. Crossref | PubMed
  22. MacDonald MR, Eurich DT, Majumdar SR, et al. Treatment of type 2 diabetes and outcomes in patients with heart failure: a nested case-control study from the U.K. General Practice Research Database. Diabetes Care 2010; 33 :1213–8.; PMCID:PMC2875425 Crossref | PubMed
  23. Boussageon R, Supper I, Bejan-Angoulvant T, et al. Reappraisal of metformin efficacy in the treatment of type 2 diabetes: a meta-analysis of randomised controlled trials. PLoS Med 2012; 9 :e1001204.; PMCID:PMC3323508 Crossref | PubMed
  24. Monami M, Dicembrini I, Mannucci E. Dipeptidyl peptidase-4 inhibitors and heart failure: a meta-analysis of randomized clinical trials. Nutr Metab Cardiovasc Dis 2014; 24 :689–97. Crossref | PubMed
  25. Savarese G, Perrone-Filardi P, D’Amore C, et al. Cardiovascular effects of dipeptidyl peptidase-4 inhibitors in diabetic patients: a meta-analysis. Int J Cardiol 2015; 181 : 239–44. Crossref | PubMed
  26. Green JB, Bethel MA, Armstrong PW, et al. Effect of Sitagliptin on Cardiovascular Outcomes in Type 2 Diabetes. N Engl J Med 2015; 373 (3):232–42. Crossref | PubMed
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Can congestive heart failure be caused by diabetes?

By American Heart Association News Please note: This article was published more than two years ago, so some information may be outdated. If you have questions about your health, always contact a health care professional. (Maskot, Getty Images) Having Type 2 diabetes or heart failure independently increases the risk for getting the other, and both often occur together, further worsening a patient’s health, quality of life and care costs, a new report says. Many of the risk factors and mechanisms behind Type 2 diabetes and heart failure are similar, yet there’s a lack of guidance on how to care for people with both conditions, according to a scientific statement from the American Heart Association and the Heart Failure Society of America published Thursday in the journal Circulation,

  • Recent studies have found new treatments for diabetes may also improve heart failure outcomes, showing the interplay between the two conditions, the report says.
  • The statement summarizes what’s known about the inner workings of diabetes and heart failure and the best ways to treat the conditions when they occur simultaneously.

But it also encourages clinicians to coordinate the care and treatment of patients who have both conditions in “a thoughtful and cohesive way,” said Dr. Shannon Dunlay, who co-chaired the report’s writing committee. It’s not uncommon for a patient to see a cardiologist for heart failure and then visit a primary care doctor or endocrinologist for help managing diabetes, she said.

But physicians need to be aware of how medications used for one condition affect the outcome of another. “There’s so much new data coming out all the time. We want to bring attention to the fact that diabetes and heart failure have substantial overlap, and it’s important to stay up to date on new information,” said Dunlay, a heart failure cardiologist at the Mayo Clinic in Rochester, Minnesota.

Ideally, all the patient’s care teams would be aligned. “It’s easy to focus on the main problem you are treating, such as heart failure. But it’s important to think about other medical conditions patients have when prescribing new therapies,” she said.

  • People who have Type 2 diabetes, characterized by elevated blood sugar levels, are two to four times more likely to develop heart failure than someone without diabetes.
  • But heart failure, a condition in which the heart fails to efficiently pump oxygenated blood through the body, also is a risk factor for diabetes.

Both disorders are characterized by insulin resistance and high levels of inflammation, said Dr. Rozalina McCoy, another member of the statement’s writing committee. “People who have both these conditions have a much higher risk of worse health outcomes – more hospitalizations, more emergency department visits, earlier death, and worse health overall than people who have just one of these conditions,” said McCoy, an endocrinologist and internal medicine physician at Mayo Clinic.

  • Since people who have either condition are at increased risk for developing the other, they should take proactive steps to improve their health, she said.
  • It’s important to get regular exercise, maintain a healthy weight and eat a well-balanced diet.
  • People with diabetes also need to keep their blood sugar levels under control.

The statement describes in detail a new class of medications called SGLT-2 inhibitors that lower blood sugar in adults with diabetes. But research shows these drugs also are effective in reducing the risk of developing heart failure and helping manage the condition in those who already have it, preventing heart failure-related hospitalizations and deaths.

Which type of heart failure is commonly associated with diabetes?

Patients with diabetes mellitus have >2× the risk for developing heart failure ( HF; HF with reduced ejection fraction and HF with preserved ejection fraction ).

Is type 2 diabetes associated with cardiovascular disease?

Skip Nav Destination Article navigation How Diabetes Cause Heart Failure Perspectives in Care | June 13 2017 Muhammad Abdul-Ghani ; 1 Division of Diabetes, University of Texas Health Science Center at San Antonio, and South Texas Veterans Health Care System, San Antonio, TX 2 Diabetes Clinical Research Center, Academic Health System, Hamad General Hospital, Doha, Qatar Search for other works by this author on: Ralph A.

DeFronzo ; 1 Division of Diabetes, University of Texas Health Science Center at San Antonio, and South Texas Veterans Health Care System, San Antonio, TX Search for other works by this author on: Stefano Del Prato ; 3 Department of Clinical and Experimental Medicine, University of Pisa School of Medicine, Pisa, Italy Search for other works by this author on: Robert Chilton ; 4 Division of Cardiology, University of Texas Health Science Center at San Antonio, and South Texas Veterans Health Care System, San Antonio, TX Search for other works by this author on: Rajvir Singh ; 2 Diabetes Clinical Research Center, Academic Health System, Hamad General Hospital, Doha, Qatar Search for other works by this author on: Robert E.J.

Ryder 5 Sandwell and West Birmingham Hospitals National Health Service Trust, Birmingham, U.K. Search for other works by this author on: 1 M.A.-G. and R.A.D. contributed equally to the development of this Perspective. Diabetes Care 2017;40(7):813–820 Hyperglycemia is the major risk factor for microvascular complications in patients with type 2 diabetes (T2D). However, cardiovascular disease (CVD) is the principal cause of death, and lowering HbA 1c has only a modest effect on reducing CVD risk and mortality.

The recently published LEADER and SUSTAIN-6 trials demonstrate that, in T2D patients with high CVD risk, the glucagon-like peptide 1 receptor agonists liraglutide and semaglutide reduce the primary major adverse cardiac events (MACE) end point (cardiovascular death, nonfatal myocardial infarction, nonfatal stroke) by 13% and 24%, respectively.

The EMPA-REG OUTCOME, IRIS (subjects without diabetes), and PROactive (second principal end point) studies also demonstrated a significant reduction in cardiovascular events in T2D patients treated with empagliflozin and pioglitazone. However, the benefit of these four antidiabetes agents (liraglutide, semaglutide, empagliflozin, and pioglitazone) on the three individual MACE end points differed, suggesting that different underlying mechanisms were responsible for the reduction in cardiovascular events.

Since liraglutide, semaglutide, pioglitazone, and empagliflozin similarly lower the plasma glucose concentration but appear to reduce CVD risk by different mechanisms, there emerges the intriguing possibility that, if used in combination, the effects of these antidiabetes agents may be additive or even multiplicative with regard to cardiovascular benefit.

Individuals with type 2 diabetes (T2D) have a twofold increased risk for cardiovascular disease (CVD) (myocardial infarction, stroke, peripheral vascular disease), and CVD is the principal cause of death in T2D patients (1). Clinical trials (2–5) consistently have demonstrated that lowering HbA 1c in T2D patients has no (2,3) or only a modest (4,5) effect on reducing cardiovascular (CV) risk.

  1. In contrast, correction of traditional CVD risk factors, e.g., blood pressure and cholesterol, markedly reduces CVD risk and mortality in patients with T2D.
  2. The recently published LEADER (Liraglutide Effect and Action in Diabetes: Evaluation of Cardiovascular Outcome Results) (6) and SUSTAIN-6 (Trial to Evaluate Cardiovascular and Other Long-term Outcomes with Semaglutide in Subjects with Type 2 Diabetes) (7) trials provide evidence that glucagon-like peptide 1 receptor agonists (GLP-1 RAs) (liraglutide and semaglutide) reduce CVD risk beyond their glucose-lowering effect and improvement in other CVD risk factors in T2D patients with established CVD.

Together with EMPA-REG OUTCOME (BI 10773 Cardiovascular Outcome Event Trial in Type 2 Diabetes Mellitus Patients) (8), IRIS (Insulin Resistance Intervention After Stroke Trial) (9), and PROactive (PROspective pioglitAzone Clinical Trial In macroVascular Events) (10)—which showed reduction in major adverse cardiac events (MACE) end points of 14%, 24%, and 16% (main secondary end point), respectively—these studies make it clear that we are entering a new era in T2D management, where the newer antidiabetes medications, in addition to lowering plasma glucose, also exert a CV protective effect that is independent of reduction in plasma glucose concentration and traditional CVD risk factors.

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Can Type 2 diabetes cause coronary heart disease?

When you have diabetes, you’re more at risk of heart disease. This is also called cardiovascular disease (CVD) or coronary disease, and can lead to heart attacks and strokes, – Cardiovascular disease affects your circulation too. And poor circulation makes other diabetes complications worse – like problems with your eyes and feet. Every week, we estimate, diabetes is a cause in over 590 heart attacks and 770 strokes in the UK

Can exercise make heart failure worse?

People with heart failure feel better when they stay active. Years ago, patients were told to rest and give up activities. But, now, research shows that normal activity is safe for most people with heart failure. Being active may help relieve your symptoms.

What percentage of diabetics have heart attacks?

The bottom line Researchers found over 90 percent of people with type 2 diabetes have a high risk of fatal heart disease or stroke within 10 years.

How does diabetes clog arteries?

Causes of diabetic arterial disease – People with diabetes have too much sugar in their blood. This may change blood chemistry and cause blood vessels to narrow. Or, it can damage blood vessels — a process known as atherosclerosis, Atherosclerosis is also called hardening of the arteries.

  • It results when plaque — which is made up of cholesterol and other fats, calcium, and fibrous tissue — builds up in the walls of arteries.
  • If enough plaque builds up to narrow or block an artery for a prolonged period, it can cause damage to tissue and organs.
  • The health problems that result depend on the location of any narrowing or blockage.

For example:

Narrowing or blockage of an artery that supplies blood to the heart can result in heart attack. Blocked carotid arteries in the neck can result in a stroke. Blockages in the blood vessels to the legs may lead to difficulty walking or wounds in the feet. The same circulation problems often occur in the arteries that supply the eyes and kidneys.

Why do diabetics have silent heart attacks?

With commentary by Elsayed Z. Soliman, M.D., MSc., M.S., study senior author and director of the epidemiological cardiology research center at Wake Forest Baptist Medical Center, Winston-Salem, North Carolina. How Diabetes Cause Heart Failure Not all heart attacks announce themselves with Hollywood-style crushing chest pain and a drenching, cold sweat. When researchers from Wake Forest Baptist Medical Center in Winston-Salem, North Carolina, checked the hearts and medical records of 9,498 people over nine years, they found1 nearly equal numbers of untreated, silent heart attacks and recognized heart attacks that had received medical attention.

A silent heart attack may be missed because the symptoms are mild or seem like another, less-urgent health issue – such as indigestion, heartburn, the flu, fatigue or an ache-y muscle – notes Elsayed Z. Soliman, M.D., MSc., M.S., study senior author and director of the epidemiological cardiology research center at Wake Forest Baptist Medical Center, Winston-Salem, North Carolina.

“People may also decide not to go to the hospital if they’re not sure it’s a heart attack, or if the hospital is far away, they don’t have health insurance or are concerned about the cost of care,” Dr. Soliman told EndocrineWeb.com. But in the study, published May 16 in the journal Circulation, that proved deadly.

People who’d had silent heart attacks were three times more likely than those who hadn’t had a heart attack at all to die. Typically, people who’ve had a silent heart attack miss out on emergency care that can save heart muscle during a heart attack such as fast treatment with procedures that open blocked arteries in the heart.

They may also miss out on stepped-up attention to blood pressure, cholesterol, diet, exercise and stress afterwards that lower risk for future problems. Dr. Soliman says silent heart attacks are a particular concern for people with diabetes. High blood sugar, high blood pressure and cholesterol problems raise risk for heart events, but nerve damage can make warning signs of an attack impossible to feel.

People with diabetes may have an impaired perception of chest pain, a key symptom that compels people to go to the hospital,” he says. The study is part of the on-going Atherosclerosis Risk in Communities research project involving white and African-American volunteers from Maryland, Minnesota, Mississippi and North Carolina.

Participants underwent electrocardiograms to measure electrical activity in the heart; abnormalities can signal that a silent heart attack has happened. Silent heart attacks seemed to be slightly more common in African-Americans than whites. They were also more common in men in general, but raised risk for future deaths more in women.

Once discovered, a silent heart attack needs aggressive treatment to prevent future attacks, Dr. Soliman says. “A silent heart attack is a heart attack,” he says. “Doctors need to help patients who have had a silent heart attack quit smoking, reduce their weight, control cholesterol and blood pressure and get more exercise.” That doesn’t mean everyone needs an EKG.

“If you are at high risk for a heart attack because you have diabetes, high blood pressure, high cholesterol, smoke or a family history of heart disease or sudden cardiac death, your doctor can determine whether or not you need one,” Dr. Soliman says.

People at high risk for heart trouble due to diabetes and other factors should also pay attention to heart-attack symptoms that whisper instead of shouting – particularly unusual fatigue, shortness of breath or pain in the chest, shoulders, arms or back that come on during regular exercise or physical work.

“Symptoms during activities you used to perform without any unusual sensations are important to watch for,” he says.1. Zhang ZM, Rautaharju PM, Prineas RJ et al: Race and Sex Differences in the Incidence and Prognostic Significance of Silent Myocardial Infarction in the Atherosclerosis Risk in Communities (ARIC) Study. How Diabetes Cause Heart Failure Sari Harrar is an award-winning freelance journalist specializing in health, medicine, and science. She writes for national magazines including Consumer Reports on Health, Good Housekeeping, Prevention, and O—Oprah magazine, and is the author of “Lower Your Blood Pressure Naturally” (Rodale, 2014).

Can you make your heart stronger if you have heart failure?

Theresa Cary MSN, RN, ACNS-BC, CHFN, CCRN, and Clinical Nurse Specialist in heart failure talks about the importance of exercise for patients with heart failure. Regular exercise has many benefits for patients with heart failure. A regular activity program will help:

  • Reduce heart disease risk factors and the chance of having future heart problems
  • Strengthen the heart and cardiovascular system
  • Improve circulation and help the body use oxygen better
  • Help increase energy levels so you can do more activities without becoming tired or short of breath
  • Improve muscle tone and strength
  • Improve balance and joint flexibility

Your doctor will let you know when it is the right time to begin an exercise program. You may need to avoid certain activities or have other restrictions based on your health. It may take many months to develop the optimal exercise program. Please refer to the heart failure binder and your personal hospital discharge plan for more information.

  1. Start slowly and gradually increase your walking pace over three minutes until the activity feels moderate (slightly increased breathing, but should still be able to talk with someone). If you feel too short of breath, slow down your walking pace.
  2. Walk at a moderate pace for about five-ten minutes the first time and each day try to add one or two minutes as you are able. You may tolerate shorter bursts of activity spread throughout the day. Aim for a goal of walking 30-45 minutes per day with rest intervals as needed; on most days of the week.
  3. Remember to cool down at the end of your exercise by gradually walking slower for the last three minute of your exercise.
  4. Rest when you need to, but try not to lie down after exercise, as it reduces exercise tolerance.
  5. If walking outside, walk with someone or in short distances close to home so you do not get too far away and have a hard time walking home.
  6. Choose an aerobic activity that you enjoy such as walking (outside or on a treadmill), stationary cycling, swimming, and rowing or water aerobics.
  7. Ask your doctor before lifting weights.
  8. Exercise should be done regularly to gain the benefits; national guidelines suggest most days of the week if not everyday.
  9. Try to exercise at the same time everyday to establish a habit and to minimize any variables that may impact your exercise (timing of meals, medications, work schedule, etc.)
  10. Remember that some shortness of breath or a faster heart rate is expected when you exercise. But – if you have excessive shortness of breath, a rapid heart rate that does not resolve after 15 minutes of rest, dizziness, chest discomfort, or weakness, stop your exercise, rest and notify your doctor.
  11. You may be on medications that may affect your exercise tolerance; keep your exercise expectations day to day as you go through recovery.

Ask your doctor about an outpatient cardiac rehabilitation program to assist with developing the best exercise program and assisting with lifestyle changes such as heart healthy diet, quitting smoking, weight loss and stress management. Cardiac rehabilitation may not be covered by insurance companies for patients with heart failure so please call your insurance company first.

Will walking help heart failure?

Know the benefits of exercise for heart failure – Over the past two decades, research has shown the positive impact of exercise training in patients with heart failure. Among the benefits are:

Feeling better – exercise improves your body’s efficiency over time, which helps to reduce heart failure symptoms. Less hospital visits – studies on exercise in heart failure patients show that a regular exercise program reduces hospitalizations and clinical events. Higher tolerance for exercise – studies have shown that heart failure patients can see improvements in their quality of life when they take part in an exercise program.

Does deep breathing help heart failure?

BACKGROUND – Prior studies indicate that doing breathing exercises improves physical performance and quality of life (QoL) in heart failure patients. However, these effects remain unclear and contradictory.

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