DM and HF

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DM is cosidered as amajor risk factor for cardiovasular disease, and it is considered as leading cause for angiopathy and related to cardiomyopathy , in this lecture I discuss the reation of DM and heart failure

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Congestive Heart Failure and Diabetes A - lethal combination by: Consultant Cardiologist Dr.Abdelsalam Sherif

Case study:

Case study A 50 yrs old patient presented with :- SOB which has recently started. Easy fatigability. No fever nor chill No special habits. With H/O of DM and HTN( several yrs) Without H/O of CAD. Physical findings:- Overweight (BMI  33) BP: 170/ 90 mmHg. Chest: bilateral basal rales. Heart: NAD. Investigations:- For further workup of dyspnea, the following investigations were done :

(1) ECG:

(1) ECG

ECG:

ECG

(2) Chest XR:

(2) Chest XR

(3) Echo-study:

(3) Echo-study

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Etiology Epidemiology Pathophysiology Diagnosis Prevention Prognosis and therapy CHF and Diabetes Mellitus

Etiology:

Etiology Risk factors  heart failure in diabetic patients:- 1) CAD 2) Arterial hypertension 3) Diabetic cardiomyopathy

Epidemiology:

Epidemiology The Framingham study firmly established the epidemiologic link between DM and HF, where, the risk of HF among diabetics: 2.5 folds in men. 5 folds in women. An overall prevalence of HF in diabetics is 12 % ( Community based studies) and > 30% of HF patients have DM ( multivariate analysis identified CHF as an independent predictor of type 2 DM).

Pathophysiology:

Pathophysiology According to ACC/AHA guidelines for management of heart failure, the presence of DM is regarded as:- 1) stage A HF (risk of HF). 2) stage B HF (structural abnormalities such as LVH without overt cardiac dysfunction LV dysfunction in DM may be Diastolic or systolic. LV diastolic dysfunction in type I DM may result from a) metabolic abnormalities. b) ↑ in FFA. c) carnitine deficiency. d) advanced glycation end products. e) changes in ca ++ homeostasis. g) insulin resistance. h) endothelial dysfunction

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While in type 2 DM, the LV diastolic dysfunction may result from:- a) cardiac autonomic neuropathy. b) apoptosis and necrosis. c) ↓ insulin-like growth factor. d) ↑transforming growth factor. e) ↑angiotensin II and aldesterone. So, mechanisms therefore occur on a myocardial, vascular and neuro-humoral level.

Endothelial dysfunction (ED):

Endothelial dysfunction (ED) ED is one of the earliest signs of vasculopathy in DM and is due to several mechanisms :- a) Inflammation. b) Oxidative stress. c) Vascular insulin resistance. ED can be assessed Indirectly by:- a) Biochemical parameters ( such as Von Willebrand factor). b) Functional assessment as by flow –mediated dilation (FMD). NB. Glitazones and statins improve endothelial – dependent vasodilatation in diabetics, while fibrates improve post – ischemic FMD of the brachial artery.

Early Detection of Heart Failure:

Early Detection of Heart Failure * History and physical examination. * Routine investigations * BNP – Sensitivity = 92% - Specificity = 72% * Graded Exercise Test. * Echocardiogram with Doppler

Prevention of HF in Diabetics, we can ?:

Prevention of HF in Diabetics, we can ? * GAMI study showed that: 34% of their patients without previously known diabetics, had a normal glucose tolerance on discharge after AMI. 35% documented to have IGT. 31% were diabetics. Recommendation : abnormal glycemia should be excluded in all AMI patients. * Several studies demonstrated the value of intensive control with multifactorial intervention through lipid, BP, and metabolic control in ↓ CV risk in diabetics

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Several ongoing trials will further clarify detection and prevention of CHF:- (1) DYDA study will examine the rate of LVD in 1000 diabetic patients without clinically documented CV disease using echo- study and BNP measurement. (2) ORIGIN trial using insulin replacement therapy in patients with IFG, IGT, or early diabetics. aiming to evaluate whether the treatment will ↓ risk of CV disease > standard approaches. starting in 2003 and final result in 2008.

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(3) NAVIGATOR trial to evaluate the effect of either insulinotropic agent (natiglinide), ARB (valsartan) or the combination on progression of IGT patients ( 7500) to diabetes and risk of CV events with final result ( end of 2007 or in 2008). NB whether more intensive metabolic control of DM can improve the outcome of patients with HF, RCT to test this hypothesis are warranted.

Prognosis:

Prognosis  Patients with diabetes and HF have a poor prognosis. Diabetic patients in SOLVD study were 1) More hospitalized. 2) Higher rates of one year of all – cause mortality ( 32% Vs 22% ) than non diabetics.  In MERIT-HF study, death or hospitalization over 1 yr occurred in 19.6% of patients overall, but ↑ to 29.2% in diabetics

Management::

Management: Symptomatic – Diuretic, ACEI or ARB digoxin, O2, rest, dietary modification. Glycemic Control: Aim to facilitates myocardium to use glucose rather than FFA as a source of energy in order to improve prognosis.

PowerPoint Presentation:

Current treatment of CHF involves pharmacotherapy that is, in most cases, not specific for the diabetic condition.  ACEI and ARBs  . ↓death . ↓HF hospitalization. Diuretics B- blockers Spironolactone Digitalis

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 Novel drugs have been disappointing for HF as:- . Omapatrilat . Endothelin antagonists.  Embryonic stem cells and endothelial progenitor cells : TOPCARE AMI trial revealed that progenitor cell transplantation may improve EF.

 Heart transplantation::

 Heart transplantation: DM is a relative contraindication to heart transplantation, however, the outcome in properly selected patients is comparable to that in nondiabetics. In 101 diabetics of 345 consecutive heart transplant recipients: 1) 5 yrs survival rate was comparable ( diabetics and non diabetics) was around 82 %) 2) Rates of infection were higher among diabetics - at 90 days ( 14% Vs 3 %). - at 4 yrs ( 29% Vs 15%).

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Glycemic Control: - UKPDS(35) have suggest that for every 1% decrement in HBA1c levels, there is a 16% relative reduction in the risk of developing HF - Aim to facilitates myocardium to use glucose rather than FFA a source of energy. * FFA utilization – following adverse effect. - Increase sympathetic activity. - Cardiotoxic. - Arrhythmogenic

Hypoglycemic drugs:

Hypoglycemic drugs * There are no prospective studies analyzing the best glucose lowering therapy in diabetic patients with HF. Insulin: ↓ blood glucose, but it may also  - ↑ myocardial blood flow. - ↓HR. - a modest ↑ in C.O. However, insulin treatment in patients with DM and HF is under debate Thiazolidendiones( TZDs) : TZDs – Reduce Insulin Resistance - Reduce risk of endothelial dysfunction. - Inflammation, microalbuminuria - Decrease LDL. - Positive effect on remodelling of myocardium.

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TZDs may  fluid retention with peripheral edema ( 2 – 5%). - Combination of glitazones and insulin had a higher incidence of HF. - The incidence of HF over 40 months was 8.2% in 5441 patients using TZDs in comparison to 5.3% in 28103 patients using other oral hypoglycemic agents. - Recommendations of TZD therapy according to the AHA/ ADA , the approach can outline as following:- 1) Diabetics without established heart disease, TZDs should be prescribed according to the package insert guidelines.

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2) The initial dose of TZDs should be low in following conditions:- a) Presence of one or more risk factors for HF. b) ↓ LVEF without sign or symptoms of HF. c) Patients with NYHA I or II HF. Precautions: I. Observation of weight gain or edema. II. Dose escalation should be performed gradually while reassessing the patient for signs of HF. 3) TZDs should not be used in patients with class III or IV HF. NB. Evidence of HF, the use of TZDs should be reconsidered as regard - dosage change . - Temporary or permanent discontinuation .

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 Metformin * HF patients who take metformin are at ↑risk of lactic acidosis especially with (1) Haemodynamic instability. (2) Other concurrent medical conditions as - renal insufficiency. - liver disease. - severe infection with reduced tissue perfusion. So, according to FDA, metformin is contraindicated in patients with HF requiring drug therapy. NB. In stable, well compensated HF patients with a s.creatinine < 2mg /dl, the risk of lactic acidosis is probably small.

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Thank you

Rosiglitazone does not adversely affect cardiac function in type 2 diabetics with heart failure :

Rosiglitazone does not adversely affect cardiac function in type 2 diabetics with heart failure The primary objective of this study was to investigate the effects of rosiglitazone on cardiac structure and function in patients with type 2 diabetes mellitus and preexisting congestive heart failure," write Dr Henry Dargie (Western Infirmary, Glasgow, Scotland) and colleagues in the April 17, 2007 issue of the Journal of the American College of Cardiology . "The results show that the use of rosiglitazone over a period of one year was not associated with any significant changes in left ventricular volumes, left ventricular ejection fraction (LVEF), or cardiac index."

Patients with other adjudicated clinical end points:

Dargie HJ et al. J Am Coll Cardiol 2007; 49:1696-704. Patients with other adjudicated clinical end points Adjudicated end point Placebo, n=114 (%) Rosiglitazone, n=110 (%) p New or worsening edema 8.8 25.5 0.005 Increase in congestive heart failure medication 17.5 32.7 0.037

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