Coronary Artery Disease in Diabetes
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  • Balkau et al. 1 analyzed the 20-year mortality of the men aged 44–55 years in the Whitehall, 2 Paris Prospective 3 and Helsinki Policemen 4 studies. 75% of the deaths in the Helsinki study were from cardiovascular disease, compared with 56% and 31% in the Whitehall and Paris studies, respectively. 1. Balkau B, et al . Lancet 1997; 350: 1680. 2. Reid DD, et al . Lancet 1974; 1: 469–473. 3. Ducitemi è re P, et al . Diabetologia 1980; 19: 205–210. 4. Pyorala K. Diabetes Care 1979; 2: 131–141.
  • Diabetic patients without previous MI have as high a risk as do nondiabetic patients with previous MI. Even after adjustments for TC, hypertension, and smoking, this relationship remains relatively constant. These data provide a rationale for treating cardiovascular risk in diabetic patients as aggressively as in nondiabetic patients with prior MI. Changes in Canadian Working Group Guidelines from interim report recommendations now classify patients with diabetes mellitus over the age of 30 years as being at very high risk for CAD.   Reference: Haffner et al. Mortality from coronary heart disease in subjects with type 2 diabetes and in nondiabetic subjects with and without prior myocardial infarction. NEJM 1998;339:229-34.
  • Slide 8. Trends in Mortality Rates for Ischemic Heart Disease in NHANES Subjects with and without Diabetes In a comparison of mean 9-year follow-up in participants in NHANES I, conducted in 1971-1975, and participants in the NHANES I Epidemiologic Follow-up Survey, conducted in 1982-1984, CHD mortality declined appreciably in nondiabetic men and women. In contrast, the decline among diabetic men was much smaller, and CHD mortality increased slightly in diabetic women, though the difference was not statistically significant. Reference: Gu K, Cowie CC, Harris MI. Diabetes and decline in heart disease mortality in US adults. JAMA 1999;281:1291-1297. http://www.ncbi.nlm.nih.gov:80/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=10208144&dopt=Abstract Keywords: coronary heart disease, diabetes, mortality, NHANES Slide type: graph
  • Putative Mechanism for Increased Atherosclerosis in Type 2 Diabetes A number of candidates have been proposed to contribute to the increased risk of CHD in diabetic patients. The precise importance of each of these mechanisms, however, is not at this point understood. Reference: Bierman EL. George Lyman Duff Memorial Lecture. Atherogenesis in diabetes. Arterioscler Thromb 1992;12:647-656.
  • A registry of patients with acute coronary syndrome (unstable angina, acute myocardial infarction: both ST elevation and non-ST segment elevation AMI) shows that both early and late adverse outcomes are more frequent in the diabetic patient. In multivariable logistic regression analyses adjusting for patient characteristics (age, gender, baseline atherosclerotic risk factors, previous MI/heart failure, previous revascularization (PCI/CABG), ECG changes at presentation, cardiac enzymes (CK and/or Troponin), Killip class, and diabetes) is independently associated with higher all-cause mortality at 1-year (Odds ratio: 1.52 (95% CI: 1.18-1.97), P<0.001), all-cause mortality and recurrent MI at 1-year (Odds ratio: 1.27 (95% CI: 1.04-1.57), P=0.022).
  • Patients with stable coronary artery disease undergoing elective PCI were found to have either known diabetes (DM), undiagnosed diabetes or impaired fasting glucose (IFG) in 62%. Long term mortality was significantly greater in patents with IFG, Undiagnosed DM and known DM. A fasting glucose of >5.5mm/L best identified patients at higher risk of cardiovascular mortality.
  • To date, approximately 3,400 patients from 186 physicians have been enrolled in the Canadian Heart Research Centre (CHRC)-coordinated Vascular Protection (VP) Registry from December 2001-2003; the number of physicians and total number of patients enrolled in each province are listed.
  • More than 55% of the patients enrolled thus far have diabetes mellitus. Patients with diabetes, as compared to those without, were younger and more likely to be women. In addition, diabetics had slightly higher systolic and diastolic blood pressures (BP), with significantly greater waist circumference and body mass index. Based on the inclusion criteria of the registry, all of the non-diabetics had some type of clinically overt vascular disease; however, even diabetics had a 10-37% frequency of peripheral vascular, cerebrovascular, and/or cardiovascular disease, identifying a very high risk group of diabetic patients.
  • *Other lipid lowering therapy use higher in diabetics, but overall therapy still lower in diabetics. + ACE inhibitor use not as high as recommended because of non-evidence based use of ARBs (Canadian Journal of Cardiology) October 2003. Since all patients in the Vascular Protection Registry are at high risk for subsequent cardiovascular events, current guidelines recommend routine use of antiplatelet (especially ASA/Aspirin ™ ), lipid lowering, and angiotensin converting enzyme (ACE) inhibitor therapies. Diabetics were more likely to receive ACE inhibitor (or angiotensin receptor blocker [ARB]) therapy than non-diabetics {right panel} at the time of enrolment (baseline), 6 months, and 1 year. However, diabetics were significantly less likely to receive antiplatelet {left panel} and statin {middle panel} therapies; although other lipid-lowering (non-statin) treatment was higher in diabetics, overall lipid-lowering therapy remains lower in diabetics, despite their high vascular risk.
  • Slide 4 Risk factors for the development of congestive heart failure were determined in the Framingham Heart Study. The hazard ratios were adjusted for age and risk factors. This slide shows the important risk factors for the development of congestive heart failure. Hypertension and previous myocardial infarction are large risk factors for congestive heart failure. Diabetes is one of the major risk factors, especially in women. Although it is true that many of these risk factors coexist with diabetes, diabetes per se is an independent risk factor of CHF.
  • Slide 5 Further evidence for the influence of diabetes on the incidence and prevalence of heart failure is provided by this study. The Kaiser Permanente Northwest Division (KPNW) diabetes registry was used to identify 9,591 registrants with diabetes diagnosed before January 1997. A randomly selected sample of 9,591 KPNW members without diabetes served as an age- and sex-matched control group. The mean follow-up period was 28 months (range: 1 to 30 months). This slide show the baseline prevalence of CHF in these populations. Those with type 2 diabetes were 2 to 8 times more likely to have CHF at baseline than those without diabetes. The incidence and prevalence of CHF increase with age and the rates of increase, about a doubling for each 10 years, are similar in the control and diabetic cohort.
  • Slide 14 The Strong Heart Study is a population-based survey of cardiovascular risk factors and disease in American Indian tribal communities in Arizona, Oklahoma, and North and South Dakota. Echocardiograms were used to determine left ventricular dimensions. Compared with nondiabetic subjects, women with type 2 diabetes had increased LV mass, increased LV wall thicknesses without a change in chamber size. Similar changes were seen in diabetic and nondiabetic men. These changes result in LV dysfunction as indicated by the reduction in midwall shortening. In this study the diabetic participants were older (60.2 vs 58.9 years), heavier (32.4 vs 28.9 BMI ), and had higher blood pressure (133/75 vs 124/74 mm Hg) than non diabetic participants.
  • Recently at the ACC, data in a large group of diabetic patients was presented using a paclitacel coated stent Diabetics did indeed appear to benefit substantially from used of this coated stent with reductions in TLR into the same range as nondiabetic patients
  • Vascular protective maneuvers are things that should be considered in any high risk patient with diabetes, before anything else is known about the patient. For example, we know in advance of meeting with a person with diabetes that we would be attempting to control blood sugar as one of the strategies to reduce their cardiovascular risk. Most of these maneuvers are strategies that have long been employed as part of the management of patients with diabetes. A non-traditional maneuver is the use of ACEi as a vascular protective maneuver, independent of the presence of hypertension, pre-existing cardiac disease or nephropathy, as supported by the MICRO-HOPE trial. STENO 2 provides support for this approach to vascular risk reduction.

Transcript

  • 1. Coronary Artery Disease in Diabetes Lawrence A Leiter MD FRCPC FACP St Michael’s Hospital University of Toronto
  • 2. Mortality Rate in DM vs Non DM Balkau B, et al . Lancet 1997; 350:1680. Control Diabetes Ratio 2.5 Ratio 2.2 Ratio 2.1 Whitehall Study Mortality rate (deaths per 1,000 patient years) Paris Prospective Study Helsinki Policemen Study 0 5 10 15 20 25 30 35
  • 3. Is Diabetes a Coronary Equivalent?
    • Fatal & nonfatal MI in Subjects with and without Type 2 DM
    H affner et al. NEJM 1998 ;339:229-34 . 0 5 10 15 20 25 30 35 40 45 50 No prior MI Prior MI 7-year incidence of fatal and nonfatal MI in 1373 nondiabetic and 1059 diabetic subjects ( p <0.001) Incidence (%) Non-DM Type 2 DM
  • 4. Non DM *Defined in 1971-1975, followed up through 1982-1984. **Defined in 1982-1984, followed up through 1992-1993. . Trends in Mortality Rates for Ischemic Heart Disease in NHANES : DM vs Non DM 17.0 6.8 -16.6% +10.7% Men, cohort 1* Men, cohort 2** Women, cohort 1* Women, cohort 2** -43.8 % -20.4% 14.2 7.6 7.4 4.2 2.4 1.9 ( P =0.46) ( P =0.76) ( P <0.001) ( P =0.12) Rate per 1000 person-years 0 5 10 15 20 Cohort 1 Cohort 2 Men Men Women Women Gu K et al. JAMA 1999;281:1291-1297 DM
  • 5. Glucose & CV Events: Meta-Regression RR RR NB: 2 h G=7.8: RR=1.58 (1.19-2.10) Fasting G=6.1: RR=1.33 (1.06-1.67) After remove any DM: P = 0.0006 for 2 h G P = 0.06 for FPG Coutinho M, Gerstein HC et al. Diabetes Care. 1999;22:233-240. 2 h Glucose Fasting Glucose
  • 6. Glucose Levels and Risk for CVD DM Cutpoint CVD Microvascular RR 1.0
  • 7. Causes of Death in Diabetes 46% 15% 11% 8% 20% CV CVA Sepsis Cancer Other Hux JE, et al. Diabetes in Ontario, an ICES Practice Atlas 2003.
  • 8. Prevalence of DM in Ontario 31%  0 1 2 3 4 5 6 7 1995 1996 1997 1998 1999 % DM
  • 9. Life Expectancy Years 0 10 20 30 40 50 60 70 80 90 100 Men Women DM No DM
  • 10. Risk of AMI - DM vs. Non-DM
  • 11. Risk of AMI - DM vs. non-DM
  • 12. Admissions for Acute Myocardial Infarction 9%  N=104,471 ( 30% DM)
  • 13. DM vs. Non DM: Adjusted Reduction in Mortality 1994-2002 McGuire D. American College of Cardiology 2004 Scientific Sessions; Mar 2004; New Orleans National Registry of Myocardial Infarction N= 1,428,596 25% 0f U.S. acute care hospitals p<0.001 44.5 Women with diabetes p<0.001 30.2 Men with diabetes p<0.001 34.2 Women p<0.001 23.5 Men p Adjusted mortality decline (%) Group
  • 14. Putative Mechanism for Increased Atherosclerosis in Type 2 Diabetes BLACK BOX
    • Dyslipidemia
    • Hypertension
    • Hyperinsulinemia/insulin resistance
    • Hemostatic abnormalities
    • Hyperglycemia
    • AGE proteins
    • Oxidative stress
    • Endothelial Dysfunction
    • Inflammation
    Adapted from Bierman EL. Arterioscler Thromb 1992;12:647-656.
  • 15. Importance of CV Risk Factors in Diabetes Eastman RC et al, Lancet , 1997;350(Supl 1):29-32 0 2 4 6 8 10 12 Odds Ratio OR - CV Death Microalbuminuria Smoking Diastolic BP Cholesterol
  • 16. Acute Coronary Syndromes in the Diabetic Patient
    • Greater propensity for plaque rupture
    • Worse outcome
      • Increased coagulation
      • Greater extent / severity of CAD
      • More pump failure
    • Worse outcome of revascularisation
  • 17. Myocardial Infarction in Diabetic Patients Prevalence of Diabetes 21% Malmberg & Ryd én, Eur Heart J 9:259, 1988 Fatal No Yes n = 341 Diabetes Hospital Fatal One-year Reinfarction one-year Mortality 60 50 40 30 20 10 0
  • 18. Oasis Study: Total Mortality 3 6 9 12 15 18 21 24 0.25 0.20 0.15 0.10 0.05 0.0 Months Event rate RR = 2.88 (2.37-3.49) RR=1.99 (1.52-2.60) RR=1.71 (1.44-2.04) RR=1.00 Malmberg K et al. Circulation 2000;102:1014–1019 . Diabetes/CVD +, (n = 1148) No Diabetes/CVD +, (n = 3503) Diabetes/CVD -, (n = 569) No Diabetes/CVD -, (n = 2796)
  • 19. FRISC II: Diabetes Not CAD Extent is the Most Important Independent Predictor of Death and MI Age Gender Hypertension Diabetes Smoking Previous Angina Previous MI ST-depression Troponin T >0.03  g/l 3-VD/LMD 0.98 0.80 1.31 2.40 0.96 1.22 1.85 1.22 1.66 1.06 RR (0.74-1.32) (0.64-0.99) (0.86-2.00) (1.47-3.91) (0.75-1.22) (0.87-1.72) (1.17-2.93) (0.80-1.86) (1.03-2.68) (0.84-1.33) NS 0.039 0.21 0.001 0.73 0.25 0.008 0.348 0.038 0.62 95% CI p Norhammer A et al . JACC 2004; 43: 585-91 0.5 1 4
  • 20. ACS and Diabetes Clinical Outcomes Up to 1 Year % of patients 1.8 3.9 7.1 8.9 7.9 14.4 14.1 21.3 P<0.0001 P=0.035 P<0.0001 P<0.0001 0 5 10 15 20 25 In-Hospital Mortality Non-fatal MI 1-y All-Cause Mortality 1-y Mortality/MI N = 3429 N = 1149 No Diabetes Diabetes Yan R , et al . Can J Cardiol 2003;19(suppl A):260A .
  • 21. Why are Diabetic Patients at Increased Risk after ACS ? (1)
    • Older
    • More female
    • Atypical symptoms
      • Dyspnoea
      • Nausea
      • Fatigue
      • Vomiting
      • Disturbance of glycemic control
    • Delayed presentation
    • Less use of proven treatment
  • 22. Causes of Adverse Outcome in Diabetic Patients with Acute Coronary Syndromes
    • Pump Failure
    • Vulnerable non-infarcted myocardium
      • Metabolism
      • Vascular
    • Re-infarction
    • Greater Comorbidity
    More vulnerable plaques Greater thrombogenicity Renal impairment Hypertension CVD, PVD  Glucose  FFA Prior silent MI More 3VD, distal disease Smaller arteries Impaired reperfusion
  • 23. Admission Plasma Glucose / Impaired GT Independent Risk Factors for Prognosis after AMI
    • 181 AMI with admission glucose < 11.1
    • OGT prior to d/c and at 3 mo.
    • Mean admission glucose 6.5 mm/L
    • Impaired glucose tolerance or undiagnosed diabetes
    • D/C 3 mo
    • IGT 35% 40%
    • New DM 31% 25%
    Norhammar et al Lancet 2002;359:2140
  • 24. Glucose Intolerance in Chronic CAD
    • Fasting glucose in 1612 pts undergoing PCI
    • 61% had Glucose Intolerance
      • Known DM 24%
      • Undx’ed DM (FG > 7.0) 18%
      • IFG (Glucose 6.1 – 6.9 mmol/L) 18%
    Muhlestein, et al. Am Ht J 2003;146:351 .
    • Mortality by Fasting Glucose (Average 2.8 yrs)
      • Normal (< 6.0 mmol/L) 1.9%
      • IFG 6.6% p=0.002
      • Undiagnosed DM 9.5% p<0.001
      • DM 11.2% p<0.001
  • 25. Use of Cardio-protective Drugs
    • Ontario Drug Benefit Program - 65 yrs and over
    ? ? ? ? % 0 10 20 30 40 50 60 70 80 90 100 BP 2+ BP ACEi Lipid 1994 1999 Target?
  • 26. CHRC Vascular Protection (VP) Registry British Columbia 26 MDs n=555 Ontario 62 MDs N=1136 Quebec 34 MDs n=508 Alberta 7 MDs n=61 Manitoba 13 MDs n=496 Saskatchewan 16 MDs n=242 Nova Scotia 8 MDs n=173 New Brunswick 10 MDs n=144 Newfoundland 10 MDs n=107 P.E.I 3,422 / 5000* patients 186 MDs enrolling December 9, 2001 – December 9, 2003 5000 patients with either/or: CAD,PAD,CVD, Diabetic patients with at least one CAD risk factor Data on file at Canadian Heart Research Centre
  • 27. Age, years* Female (%) Systolic BP mm Hg* Diastolic BP mm Hg* Waist circumference (cm) Body Mass Index (kg/m 2 ) Coronary artery disease (%) Prior MI (%) Prior PCI or CABG (%) Cerebrovascular disease (%) Peripheral vascular disease (%) Diabetes n=1,871 (55.8%) 65 (55,72) 38 132 (122,144) 78 (70,80) 104 (95,113) 31 (27,35) 37 22 18 13 10 No Diabetes n=1,482 (44.2%) 68 (60,76) 31 130 (120,140) 76 (70,80) 98 (90,106) 28 (25,31) 82 49 43 20 13 CHRC Vascular Protection Registry: DM vs Non DM *Median (25 th , 75 th percentiles) + All comparisons p  0.004 Data on file at Canadian Heart Research Centre
  • 28. 71.9 79.3 82.8 86.3 86 89.5 0 20 40 60 80 100 Baseline 6 Months 1 Year p<0.01 p<0.01 p<0.01 % of Patients 65.9 71.2 74.9 77.2 80.1 79.6 Baseline 6 Months 1 Year p<0.001 p<0.001 % of Patients 67.9 68.3 70.2 61.9 62.1 60.6 Baseline 6 Months 1 Year p<0.01 p<0.01 p<0.01 % of Patients Antiplatelets Statins ACE Inhibitors Diabetes No diabetes CHRC Vascular Protection Registry: DM vs Non DM Data on file at Canadian Heart Research Centre
  • 29. ACS and Diabetes Early In-hospital Management % of patient S 7.6 90.9 89.3 94.5 N = 3429 N = 1149 P < 0.001 P < 0.005 Reperfusion Antiplatelet Heparin GpIIb/IIIa inhibitor 5.2 91.4 P<0.05 62.8 50.3 P < 0.001 0 10 20 30 40 50 60 70 80 90 100 Non-DM DM
  • 30. ACS and Diabetes In-hospital Cath / Revasc % of Patient 12.7 36.4 18.0 41.0 N = 3429 N = 1149 P =0.006 P < 0.001 4.0 3.8 0 5 10 15 20 25 30 35 40 45 Angio PCI CABG Non DM DM
  • 31. ACS and Diabetes Medication Use at Discharge % of patients N = 3429 N = 1149 90.3 76 73.6 52.1 65.6 36.3 53.9 54.5 P=0.008 P=0.10 P<0.0001 P<0.0001 25.2 87.5 Anti-platelet Beta ACE-I Ca Channel Lipid Blocker Blocker lowering 0 10 20 30 40 50 60 70 80 90 100 Non-DM DM
  • 32. Risk for the Development of CHF –Framingham Study Hazard Ratio HTN MI Angina Diabetes LVH Valvular Heart Disease Levy, D, et al. JAMA . 1996; 275: 1557-62. Risk Factor
  • 33. Congestive Heart Failure Is More Common in Patients With Type 2 Diabetes Age at Baseline Nichols, GA, et al. Diabetes Care . 2001; 24: 1614-9 <45 <45 95+ 95+ CHF present in 14% DM subjects at inception with 8% new cases over 5 years
  • 34. Impact of Diabetes on Risk for New CHF Following Acute Coronary Syndromes: OASIS Event Rate Malmberg K et al. Circulation. 2000;102:1014-1019 .30 .20 .15 0 3 12 18 24 Months Diabetes(+) and CVD(+) No Diabetes and CVD(+) RR= 3.43 (2.85-4.13) .05 .10 .25 6 9 15 21 0 Diabetes(+) and CVD(-) No Diabetes and CVD(-) RR= 2.19 (1.86-2.58) RR= 1.98 (1.52-2.57) RR= 1.00 Total mortality 18 10 1.57 <0.001 CVD death 14 8 1.49 <0.001 New MI 12 9 1.34 <0.001 Stroke 5 3 1.45 0.009 New CHF 21 12 1.41 <0.001 Parameter DM No DM Adjusted RR (95% CI) P Event Rate and RR for Long-term Outcomes Crude Event Rate
  • 35. Left Ventricular Mass Increases With Deteriorating Glucose Tolerance, Especially in Women : Independence of Increased Arterial Stiffness or Decreased Flow-Mediated Dilation The Hoorn Study Diabetes Care 2004; 27: 522-529 Impact of Glucose Intolerance and Insulin Resistance on Cardiac Structure and Function: Sex-Related Differences in Framingham Study Circulation 2003; 107: 448-454 Across The Range of Glucose Tolerance, Women Have Greater LV Mass and More Diastolic Dysfunction Than Men
  • 36. Impact of Diabetes on Cardiac Structure and Function in Women: Strong Heart Study Devereux, RB et al, Circ 2000: 101; 2271-2276 mean ± SD 0.87 ± 0.11 0.82 ± 0.09 4.81 ± 0.42 78 ± 16 18.4 ± 2.1 Glucose-Tolerant Women (n = 478) <0.0001 <0.0001 NS <0.0001 <0.0001 0.95 ± 0.13 0.87 ± 0.10 4.85 ± 0.48 85 ± 21 17.3 ± 2.5 Septum Thickness, cm LV Wall Thickness, cm LV Diameter, cm LV mass (g/m 2 ) LV Performance, % Shortening p DM Women (n = 1227)
  • 37. Hospitalization for Heart Failure in the Presence of a Normal Left Ventricular Ejection Fraction J Am Coll Cardiol 2004; 43: 1432-1438
    • Prospective identification of patients admitted with “pure” CHF and EF>50% in NY Heart Failure Registry
      • 619 patients
      • 73% women
      • Women 8 years younger than men
      • Co-morbid conditions
        • -Hypertension 78%
        • -Diabetes 46%
        • -Obesity 46%
        • -CAD 40%
        • -Increased LV Mass
    Diabetes and/or insulin resistance syndromes underlie most cases of non-systolic CHF, particularly in women
  • 38. Impact of Insulin Resistance on Myocardial Metabolism: Importance of FF Acid Generation Adapted from Oliver MF, Opie LH, Lancet 1994; 343: 155 CV Stress Catechols, Cortisol  Lipolysis  Plasma FFA Glucose   Insulin Coronary Occlusion Lysophospholipids Ca 2+ overload Enzyme loss  Glycolysis  Glucose Oxidation Membrane Damage Arrhythmias Phospholipids TG FFA Acyl CoA Acylcarnitine
  • 39. DIGAMI: Benefit of Tight Glycemic Control in AMI: Major Benefit in “No Insulin - Low Risk” Cohort 0 0.1 0.2 0.3 0.4 0.5 0.6 0.7 1 Malmberg, K et al BMJ 1997; 314: 1512-1515 Insulin-glucose Infusion Control Mortality Years in Study n = 314 n = 306 0 2 3 4 5 p = .0111 0 0.1 0.2 0.3 0.4 0.5 0.6 0.7 1 Insulin-glucose Infusion Control Mortality Years in Study n = 133 n = 139 0 2 3 4 5 p = .004 Total Cohort No Insulin - Low Risk 19% @ 1 year 26% CHF accounted for 66% of all deaths
  • 40. Coronary Revascularisation in DM
    • No increase in CABG operative mortality
      • Greater peri-op morbidity: wound, renal failure
    • Worse long term out-look after CABG
    • PCI: More re-stenosis over first 6/12
    • PCI: Complete revascularisation often not achieved
  • 41. DM: Mortality Rates in RCTs Comparing CABG vs. Coronary Angioplasty Koon-Hou Mak et al. European Heart Journal 2003; 24: 1087-1103 0 5 10 15 20 25 30 35 40 45 50 EAST BARI CABRI ERACI Overall Coronary Angioplasty CABG Mortality (%) 8 yr 7 yr 4 yr yr
  • 42. DM still has Worse Prognosis Post PCI in Modern Era
    • PRESTO Study
    • 11,482 patients
    • 43% diabetic
    • Tested tranilast to prevent restenosis
    • Compared out-come in DM vs Non-DM
    • 9 month follow-up
    Mathew V et al Circulation 2004;109:10 Adjusted Relative Risk DM worse Death MI TVR 0 1 2 3 Death MI TVR Comp
  • 43. Reduced Target Vessel Restenosis (TVR) after PCI Outcomes in Diabetes with TAXUS Coated Stents TAXUS IV Stone et al, Late Breaking Clinical Trials ACC, 2003 0 2 4 6 8 10 12 14 16 18 20 No Diabetes Diabetes Oral Meds Diabetes Insulin TVR (%) Control TAXUS
  • 44. Reasons for Increased Vascular Risk in DM
    • Accelerated Atherosclerosis
    • Underutilization of Evidence Based
    • Therapies
    • Altered Cardiac Metabolism
    • Unrecognized DM
    • Increased Restenosis Post PCI
  • 45. Diabetes Confers a Doubling of Risk for Early MI Mortality Despite Advances in Cardiac Care Early Mortality from Acute MI Pre-CCU Era (pre-1962) CCU Era (1962-1984) Lytic Era (1984-2000) Diabetes Total Group Defibrillation Hemodynamic Monitoring Thrombolysis Beta-blockade Aspirin PCI Era (2000-- ) PCI IIbIIIa Inhibitors Clopidrogel Statins Digoxin Diuretics From Richard Nesto
  • 46.
      • In all Patients
        • ACE inhibitor
        • ASA
        • Lipid Control (statin)
        • BP Control
        • Also as required:
          • Glycemic control
          • Lifestyle
          • Smoking cessation
    CDA Guidelines - Cardiorenal Prioritization 3. Control of Nephropathy 2. Hypertension Control 1. Vascular Protection
  • 47. Risk of CAD in DM
    • Risk of CAD in persons with DM is increased but there is recent evidence suggesting that we are beginning to turn the tide
    • Pathophysiology of accelerated atherosclerosis is multifactorial
    • Undertreatment is responsible for some of the increased vascular risk in diabetes despite proven benefit of evidence based therapies in DM
    • Antihyperglycemic treatments may also impact on CV outcomes in DM
    Conclusions :