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THE 6TH HIGHLANDS AND CENTRAL VIETNAM CONGRESS OF Click to edit Master text styles CARDIOLOGY
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Hypertension in diabetic patients

Update and Pratical Clinical Applications
CANADA-CHEP 2010, AHA 2010 ADA 2011 & WISCONSIN DMECG 2011

Prof. Nguyen Hai Thuy. MD,PhD Hue College of Medicine and Pharmacy Hue City-VietNam

I.INTRODUCTION
Hypertension (HTN) a common comorbidity of diabetes, affecting the majority of patients, with prevalence depending on type of diabetes, age, obesity, and ethynicity The prevalence of HTN in adults with DM is 20 60%, which is 1.53 times higher than that in agematched individuals without DM. Nguyen hai Thuy, Huynh Van Minh (2000-2002, Hue City ) : (490 diabetic in-outpatients, BP140/90 mmHg): HTN : 29.91%

HTN in T1DM
There is a relationshipbetween the prevalence of HTN and increasing albuminuria (study of 981 type 1 diabetic patients for five or more years) HTN was present in 19 % of patients with normoalbuminuria, 30 % with microalbuminuria, and 65 % with macroalbuminuria. 75 to 85 % with progressive diabetic nephropathy The incidence of HTN rises from 5% at 10 years, to

HTN in T2DM

HTN co-exists with type II in 40% at age 45 and 60% at age 75. A series of over 3500 newly diagnosed type 2 diabetic patients 39% were already hypertensive.

II. PATHOPHYSIOLOGY OF HYPERTENSION Click to edit Master text MELLITUS IN THE DIABETES styles
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Diabetes: A New Paradigm?

Glycemic Variability

Epidemiologic studies provide evidence for coexistence of HTN and DM and possibly point towards a common genetic and environmental factor promoting both DM and HTN. Similarly, clustering of HTN, insulin resistance or frank type 2 DM, hyperlipidaemia and central obesity have been documented in several populations.

Inhibition of glucose oxidation by FA utilization. Click to edit Master text styles

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insulin receptor substrate (IRS) , protein kinase-B (PKB). pyruvate dehydrogenase (PDH), Phosphofructokinase-1 (PFK1),

FATTY ACIDS AND INSULIN ClickRESISTANCE to edit Master text styles

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Cardiovascular targets and actions of insulin.

Muniyappa R et al. Endocrine Reviews 2007;28:463-491

2007 by Endocrine Society

Pathway-selective insulin resistance in PI3K signaling creates imbalance between prohypertensive and antihypertensive vascular actions of insulin exacerbated by compensatory hyperinsulinemia.

Muniyappa R et al. Endocrine Reviews 2007;28:463-491

2007 by Endocrine Society

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Alternative pathways whereby compensatory hyperinsulinemia contributes to myocyte hypertrophy

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Fat Cell Products and Hypertension

Visceral Fat Stores
Portal FFA Hepatic Insulin Clearance Plasma Insulin

Vascular Constriction Angiotensin II Angiotensinogen Angiotensin I

Bray GA. Contemp Diagn Obes. 1998.

Renal Na+ Reabsorption

Hypertensio n

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Insulin resistance, increased tissue inflammation and reactive oxygen species (ROS) production resulting in Endothelial dysfunction, Increased tissue reninangiotensinaldosterone system (RAAS) and Increased sympathetic nervous system (SNS) activity have all been implicated in this complex pathophysiology of DM and HTN.

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Unique aspects of HTN in diabetic patients Salt sensitivity and volume expansion
Isolated systolic HTN Loss of nocturnal decline of BP Microalbumine Orthostatic hypotension

III.Screening and diagnosis Hypertension in diabetic patients

III.Screening of Measurement of BP in the office should be hypertension

done by a trained individual and should follow the guidelines established for nondiabetic individuals: Home BP self-monitoring 24-h ambulatory BP monitoring may provide additional evidence of white coat DIABETES CARE, VOLUME 34, SUPPLEMENT 1, JANUARY 2011 and masked HTN and other discrepancies between office and true BP.

"White coat hypertension"

Click to edit Master text styles Second level Puig JG (1995) : WCH : 51% (43 diabetic patients, Third level mean age, 57 years) Fourth level Nielsen F (1997) : WCH 23% ( 30 diabetic Fifth level patients, mean age, 61 years)

Recommendations: Hypertension/Blood Pressure Control

Screening and diagnosis Measure blood pressure at every routine diabetes visit If patients have systolic blood pressure 130 mmHg or diastolic blood pressure 80 mmHg
Confirm blood pressure on a separate day
ADA. VI. Prevention, Management of Complications. Diabetes Care 2011;34(suppl 1):S27. Repeat systolic blood pressure 130 mmHg or diastolic blood pressure 80 confirms a diagnosis of hypertension (C)

Blood Pressure and Target Organ Damage (TOD)

24-h blood pressure correlates most closely with TOD Current evidence suggests (compared to clinic or casual BP) Higher incidence of cardiovascular events when blood pressure remains elevated at night (non-dippers) Blood pressure variability is an independent determinant of TOD Highest incidence of cardiovascular events occurs in AM

that:

Adapted from: Sokolow, et al. 1966; Devereux, et al. 1983; Devereux, et al. 1987; Parati, et al. 1987; Mancia. 1990.

Elderly Diabetic Patients Blood pressure must be measured in older patients with special care as some older persons have pseudohypertension (falsely high sphygmomanometer readings) due to excessive vascular stiffness as determined for example by using pulse wave pressure.

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Medial vascular calcification in diabetesClick to edit Master text styles mellitus

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Arterial stiffness Increased central aortic pressure and left ventricular afterload and lowered central diastolic and coronary perfusion pressures, leading to

Doppler Measurements Ultrasound Doppler

In order to know where along the beam the blood flow data

The flow velocity is obtained from the spectral

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Ankle-brachial edit Master text styles Click to Index (ABI)

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IV.Classification of hypertension in diabetes

1.Primary, or essential, HTN is the most common type of HTN in persons with DM. Its cause is unknown.

There are 3 categories of HTN in diabetic patients

2.Secondary HTN, which includes HTN associated with diabetic renal disease as well as HTN from other diseases, contributes to 5% to 10% of the cases.

Evaluation for secondary causes of HTN if: BP resistant to three or more antihypertensive agents, worsening control in previously wellcontrolled patient, severe HTN (>180/110 mmHg), significant hypertensive target organ damage, onset in adults <20 years or

Identifiable causes of hypertension

Chronic kidney disease Coarctation of the Aorta Cushings Syndrome Drug induced Obstructive uropathy Pheochromocytoma Primary aldosteronism and other mineralocorticoid excess states Renovascular HTN stenosis and fibromuscular dysplasia Sleep Apnea Thyroid (either HYPER or HYPO) or parathyroid disease

RENAL ARTERY STENOSIS CAPTOPRILS TEST Click to edit Master text styles
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Doppler sonography in renal artery stenosis

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Color Doppler image demonstrating normal intrarenal vasculature

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V. CVD risk factors associated with HTN in diabetic patients

Central obesity Family history Male sex or postmenopause state Cigarette smoking Physical inactivity Insulin resistance/hyperinsulinemia Microalbuminuria Dyslipidemia :TG,HDL.C, non-HDL.C

CRP

Endothelial dysfunction fibrinogen PAI-1 homocystein noctural dipping of BP and heart rate Salt sensitivity Left ventricular hypertrophy

Pathways to Cardiovascular Morbid Events

LV Dysfunction

Devereux and Alderman: Circulation ereux and Alderman: Circulation 1993;88:1444-1455. 1993;88:1444-1455

Pathways to Cardiovascular Events in Diabetes: Lessons from the Strong Heart Study

LV Dysfunction

CV Events CV Death

Adapted from Devereux and Alderman: Circulation 1993;88:1444-1455.

Noninvasively Measurable Manifestations of Preclinical Cardiovascular Disease

ereux and Alderman: Circulation 1993;88:1444-1455.

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Atherosclerotic carotid artery in hypertensive diabetic patient Nguyen hai Thuy, Pham Gia Khai, Le Huy Lieu (1994Click to edit Master text styles 1996) Second level Third level Fourth level Fifth level

FMD (Flow Mediated Dilation)

2. Left ventricular hypertrophy (LVH)

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Cornell voltage x QRS duration: (RaVL+SV3 [+ 6 mm in women]) x QRS duration. LVH > 2,440 mm*msec.

(10 mm + 19 mm + [6 mm for woman]) x 100 msec = 3500 mm*msec

Okin PM et al. JACC 1995;25:417-23.

LEFT VENTRICULAR HYPERTROPHY ANATOMY and ECHO

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LVMI in type 2 diabetic patients

Tran Thi Van Anh,Nguyen Hai Thuy, Nguyen Anh Vu (2006-2007)

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( male >125g/m2level female > 110 g/m2) was 40% and Third

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Diastolic dysfunction Screening the diabetic cardiomyopathy by evaluating diastolic function

Echocardiography study of 48 hypertensive type 2 diabetic patients (Nguyen Hai Thuy, Nguyen Quoc Viet-2003) Prevalence of diastolic dysfunction : 81,25% in which first degree was 70,83%

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Raev D.C. (1994) : diastolic dysfunction more frequent and early than systolic dysfunction in type 1 diabetic patients Poirier P and al (2001) : study of diastolic dysfunction in diabetic patients without HTN showed that diabetic cardiopathy is special cardiomypathy, independent with CAD

3. SYSTOLIC DYSFUNCTION
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Definition of Abnormal Albuminuria in Microalbuminuria Diabetes MellitusMacroalbuminuria

(Nephropathy)

Detected by dipstick

No

Yes

Urine Albumin / Cr Renal Risk

30 - 299 mg Alb / g Cr Marker of future nephropathy in some

> 300 mg Alb / g Cr Marker progressive renal disease Increased

Cardiovascular Risk

Increased

* Random (Spot) urine preferably A.M. recommended

2005. American College of Physicians. All Rights Reserved.

Management of hypertesion in diabetic patients

Management
In patients with DM, the Joint National Committee on the Detection, Evaluation, and Treatment of High Blood Pressure (JNC 7), and ADA 2011 recommends a target BP of <130/80mmHg in order to prevent death and disability associated with high BP. < 125/75 mmHg in diabetic patient with

Recommendations: Hypertension/Blood Pressure Control

Goals A goal systolic blood pressure <130 mmHg is appropriate for most patients with diabetes (C) Based on patient characteristics and response to therapy, higher or lower systolic blood pressure targets may be appropriate (B)

ADA. VI. Prevention, Management of Complications. Diabetes Care 2011;34(suppl 1):S27.

Patients with diabetes should be treated to a diastolic blood pressure <80 mmHg (B)

Recommendations: Hypertension/Blood Pressure Control

Treatment (1) Patients with a systolic blood pressure 130 139 mmHg or a diastolic blood pressure 80 89 mmHg May be given lifestyle therapy alone for a maximum of 3 months If targets are not achieved, patients should be treated with the addition of pharmacological agents (E)
ADA. VI. Prevention, Management of Complications. Diabetes Care 2011;34(suppl 1):S27.

Recommendations: Hypertension/Blood Pressure Control

Treatment (2) Patients with more severe hypertension (systolic blood pressure 140 mmHg or diastolic blood pressure 90 mmHg) at diagnosis or follow-up Should receive pharmacologic therapy in addition to lifestyle therapy (A)

ADA. VI. Prevention, Management of Complications. Diabetes Care 2011;34(suppl 1):S27.

Recommendations: Hypertension/Blood Pressure Control

Treatment (3) Lifestyle therapy for hypertension Weight loss if overweight DASH-style dietary pattern including reducing sodium, increasing potassium intake Moderation of alcohol intake Increased physical activity (B)
ADA. VI. Prevention, Management of Complications. Diabetes Care 2011;34(suppl 1):S27.

Table 3. Lifestyle Modifications to Manage Hypertension*

Impact of a 5 mmHg ReductionReduction Overall

Stroke Coronary Heart Disease All Cause Mortality 14% 9% 7%

Hypertension 2003;289:2560-2572.

In general, diabetic patients with HTN need more than one type of medication. The choice of antihypertensive drug should be determined by the drugs capacity to (1) lower blood pressure, (2) protect the diabetic patients kidneys from ongoing injury, and (3) avoid side effects.

Pharmacotherapy

ACE inhibitors & ARBs

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Angiotensin Converting Enzyme Inhibitors ( ACE-I) improve insulin sensitivity, retard the progression of diabetes and even prevent the development of diabetes in hypertensive patients by inhibiting RAAS.

Angiotensin Receptor Reducing the progression of diabetes and Blockers (ARBs)

carry other cardiovascular and renal benefits noticed in ACE-I, by virtue of its RAAS blockade.

Have beneficial effects on glucose metabolism that are likely independent of bradykinin-mediated mechanisms. LIFE study, losartan reduced the relative risk of developing type 2 diabetes by 25%

Angiotensin Receptor Reduction in the relative risk of Blockers (ARBs)

developing diabetes was noted in the Candesartan in Heart failure: Assessment of Reduction in Mortality and morbidity (CHARM) studies. The Valsartan Antihypertensive Longterm Use Evaluation (VALUE) trial demonstrated the advantage of an ARB, valsartan, over a calcium channel

Beta-blockers
Carvedilol has been shown to induce vasodilatation and improve insulin sensitivity produces less aggravation of hyperglycemia and hyperlipidemia. Recommendations for persons with DM who are taking beta-blockers include testing blood glucose often and treating hypoglycemia when blood glucose is 70

Diuretics
Thiazides have been shown to cause electrolyte imbalances, metabolic changes and volume contraction. ALLHAT, which compared a thiazide (chlorthalidone) with a calcium channel blocker (CCB) (amlodipine) or an ACE-I (lisinopril), found that the thiazide was less expensive and superior to the ACE-I or CCB in lowering the incidence of CVD in hypertensive populations.

Diuretics
Hydrochlorothiazide or chlorthalidone could be considered as a firstline therapy for many diabetic patients with HTN, despite the fact that they may adversely affect insulin resistance and potassium balance in some individuals. Treating volume expansion with thiazide diuretics can increase the activity of the RAAS. Thus, combining a diuretic with an ACE-I or an ARB can be an effective BP lowering combination. It has been shown that the unfavorable effects of thiazide diuretics on lipid and glucose metabolism are dose related and do not generally occur if low doses are used.

Calcium Channel Blockers ( A dihydropyridine CCB (amlodipine) was CCBs) used in the ALLHAT trial.
Nondihydropyridine CCBs (such as verapamil and diltiazem) may help to reduce albumin excretion and coronary events. The nondihydropyridine group, which also lowers heart rate, has been shown to give additional protection to the kidneys, when combined with ACE inhibitors.

Adrenergic (Alpha-1) Blockers The use of adrenergic (alpha-1) blockers

(such as prazosin, terazosin, and doxazosin) in diabetic patients with HTN has been controversial. The adrenergic (alpha-1) portion of the ALLHAT study was discontinued because of a high rate of complications. These drugs are still considered

Metabolic modulators
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FFAs are mobilized from adipose tissue to inhibit the uptake of glucose by muscle (including heart muscle). The result is hyperglycemia and increased insulin resistance. Elevated FFAs also act on mitochondria (mito) to cause excess oxygen wastage with formation of ROS. The consequences include mitochondrial and cellular dysfunction (ionic changes, increased cell calcium and sodium). Metabolic interventions decrease insulin resistance, hyperglycemia, and ROS formation to decrease the

Table 1. Clinical Trials of BP Medications in Patients With Diabetes Study n Follow- BP (mmHg) Drugs Impact on Up Tested Outcomes Period (years) UKPDS 5,102 20 Tight goal 150/85 versus less stringent goal < 180/105 Tight: Favors tight captopril or control: decreased atenolol death from diabetes, stroke, and microvascular disease (retinopathy) Diastolic goal Calcium < 80 group: 80 versus channel decreased major 90 blocker plus cardiovascular

HOT

18,790 3.8

Table 1. Clinical Trials of BP Medications in Patients With Diabetes Study N FollowUp Period (years) BP (mmHg) Drugs Tested Impact on Outcomes

HOPE, MICROHOPE

9,297 3.5 (4.5) Mean BP for (3,577 with both groups diabetes) 139/79 at baseline 42,418, (13,101 with diabetes) 4.9 Mean BP 146/83 at baseline

Ramipril versus placebo

Ramipril group (136/76 mmHg): decreased MI, stroke, cardiovascular death, and allcause mortality; decreased nephropathy

ALLHAT

Amlodipine Chlorthalidone group: lower versus systolic BP than amlodipine or lisinopril lisinopril; no difference for versus fatal/nonfatal MI; increased heart chlorthalido failure with amlodipine and ne lisinopril versus chlorthalidone

Table 1. Clinical Trials of BP Medications in Patients With Diabetes Study n Follow- BP (mmHg) Drugs Impact on Outcomes Up Tested Period (years) ABCD 470 5 Diastolic goal: Nisoldipine Intensive: decreased death; no difference intensive < 75 versus enalapril for retinopathy or versus neuropathy; increased moderate < MI with nisoldipine 8089 versus enalapril; renal function stabilized with both drugs ACCORD 4,73 4.7 BP 3 Systolic goal Stepped No difference in < 120 versus care to nonfatal MI, nonfatal < 140 reach goals stroke, or cardiovas

Recommendations: Hypertension/Blood Pressure Control

Treatment (6) In pregnant patients with diabetes and chronic hypertension
Blood pressure target goals of 110129/6579 mmHg are suggested in interest of long-term maternal health and minimizing impaired fetal growth

ACE inhibitors, ARBs, contraindicated during pregnancy (E)

ADA. VI. Prevention, Management of Complications. Diabetes Care 2011;34(suppl 1):S27.

During pregnancy, treatment with ACE inhibitors and ARBs is contraindicated, since they can cause fetal damage. Chronic diuretic use during pregnancy has been associated with restricted maternal plasma volume, which might reduce uteroplacental perfusion. Antihypertensive drugs known to be effective and safe in pregnancy include

DIABETIC HEART DISEASE IN HYPERTENSIVE DABETIC PATIENTS

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DIABETIC CARDIOMYOPATHY (DCM) and DIABETIC HEART DISEASE (DHD)

Marwick, Heart 2004

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Changes in Myocardial Structure

Myocellular and Interstitial Fibrosis
The extent and frequency of diastolic dysfunction is directly proportional to the HbA1c level HYPERGLICEMIA (Devereux et al. Circulation Accumulation of AGEs 2000) Disturbed Ca++ handling Cross linking of collagen FIBROSIS DIASTOLIC DYSFUNCTION Bell Diabetes Care 2003

Fibrosis

Hypertrophy

Hypertensive heart disease

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Hypertens ive heart disease

Potential factors to influence coronary reserve in hypertensive heart disease.

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Primary mechanism Functional consequences 1.Increased myocardial Increased basal O2 consumption mass Reduced coronary reserve 2.Myocardial and Increased extravascular force and periarteriolar fibrosis reduced vascular lumen Increased coronary resistance 3.Decrease in capillary Increased coronary resistance density per Reduced coronary reserve cardiomyocyte unit area Increased diffusion distance (rare- faction of the Reduced supply of nutrients to myocytes vascular bed)

4.Vascular medial Decreased vascular lumen hypertrophy with lumen Increased coronary resistance

Positron Emission Tomography

Technology of choise to assess microvascular function
Quantitative Imaging of Microvascular Function (Myocardial Blood Flow MBF)

MBF (ml/min/g)
, Bellina et al., J Nucl Med 1990

Microvascular Dysfunction in Idiopathic DC

75% of pts with microvascular dysfunction
Patients with more Severe Microvascular Dysfunction are at Increased Risk of Death and/or Heart Failure
MBF > 1.36 P = 0.0012 MBF < 1.36

Increased relative risk of 3.5 times in yrs Dip5MBF < 1.36 ml/min/g

Neglia et al., Circulation 2002

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Natural History of Diabetic Nephropathy Albuminuria Hypertension

Albumin-rich filtrate
Podocytes Foot process

Glomerular Basement Membrane

Damaged Endothelium

Time Declining GFR

GFR

Albumin Leak

CV Risk (fold )

BP

Cardiovasc ular 20 Death Risk

15 10 5

1 0 20 40 60 80 100

GFR
ESRD

Time
2005. American College of Physicians. All Rights Reserved.

Progression of Diabetic Nephropathy Diagnosis

Chronology Pathology
Stage 1 Stage 2 Stage 3 Stage 4 Stage 5
ESRD after 25-30 years
UAE = Urinary albumin excretion
Mogensen CE. Diabetologia. 1999;42:263-285.

Present at diagnosis of diabetes Within first 5 years After 6-15 years (~35% patients) After 15-25 years (~35% of patients)

Increased kidney and glomerular size Basement membrane thickening Further basement membrane thickening, mesangial expansion Clear, pronounced abnormalities proteinuria Glomerular closure, advanced glomerulopathy

and Screening
Mean arterial BP normal Normal BP or slight elevation (1 mm Hg/year) UAE = 20-200 g/day BP >3 mm Hg/year GFR decline ~10 mL/min/year BP >5 mm Hg/year GFR <10 mL/min BP >5 mm Hg/year

Diabetic Nephropathy Management

Parameter Lower BP Block RAAS Improve glycemia . Lower LDL cholesterol.. Anemia management ... Endothelial protection Smoking..

Target < 130/80 mmHg ACEi or ARB to max tolerated A1c < 6.5% (Insulin/TZD) < 100 (70) mg/dl statin + other Hb 11-12 g/dl (Epo + iron) Aspirin daily Cessation

2005. American College of Physicians. All Rights Reserved.

Diabetic Nephropathy: What about proteinuria?

Lower BP to goal with max dose ACEi or ARB Consider Adding: ACEi to ARB, mineralocorticoid receptor antagonist to ACEi or ARB Calcium Channel Blockers Non-dihydropyridine Dihydropyridine

2005. American College of Physicians. All Rights Reserved.

George L. Bakris, James R. Sowers. ASH Position Paper: Treatment of Hypertension in Patients With Diabetes An Update THE JOURNAL OF CLINICAL HYPERTENSIONVOL. 10 NO. 9 SEPTEMBER 2008

CONCLUSIONS

LV Dysfunction

CV Events CV Death

Optimal control of glycemia, BP, lipids, regimens optimized to reverse LVH, dysfunction & plaque

ed from Devereux and Alderman: Circulation 1993;88:1444-1455.

Thank you for your attention