9. People with concomitant hypertension & dyslipidemia 90 million with dyslipidemia JNC 7. May 2003; Third National Health and Nutrition Examination Survey, 1988-1994, NHANES III. 27 million with concomitant hypertension, dyslipidemia 50 million with hypertension
10. People with concomitant hypertension & dyslipidemia 9 million diagnosed (33%) 18 million undiagnosed (67%) Third National Health and Nutrition Examination Survey, 1988-1994, NHANES III.
11. People with concomitant hypertension & dyslipidemia Source: Unpublished data from the Third National Health and Nutrition Examination Survey (NHANES-III), CDC 1994; data from 1999.
12. People with concomitant hypertension & dyslipidemia 10% Treated For Hypertension & Dyslipidemia Source: Unpublished data from the Third National Health and Nutrition Examination Survey (NHANES-III), CDC 1994; data from 1999. 3% at Goal
13. Co-prevalence of dyslipidemia & hypertension in India The prevalence of coexistence of dyslipidemia and hypertension in patients surveyed at Apollo Hospitals (n=501) Indian Heart Journal 1996: 48(4): 371-374 0 10 20 30 40 50 Percent 60 70 80 90 100 0 TC>200 mg/dl (n=501) LDL>130 mg/dl (n=486) HDL<35 mg/dl (n=501) TG>200 mg/dl (n=496) TC/HDL ratio>4.5 (n=500)
14. MRFIT - Hypertension and Dyslipidemia and CAD Risk Adapted from Neaton JD, et al. Arch Intern Med . 1992;152:56-64. Age-adjusted CAD death rates
27. MRFIT - Effect of Systolic & Diastolic BP on CHD Mortality *Men aged 35-57 years followed for a mean of 12 years. <120 120-139 140-159 160+ CHD Death Rate per 10,000 Person-Years 48.3 37.4 34.7 43.8 38.1 80.6 31.0 25.5 24.6 25.3 25.2 24.9 Systolic BP (mm Hg) Diastolic BP (mm Hg) Neaton et al. Arch Intern Med . 1992;152:56-64. 100+ 80-89 70-74 <70 75-79 90-99 23.8 16.9 13.9 12.8 12.6 11.8 20.6 10.3 11.8 8.8 8.5 9.2 Patient in Question # 1
37. Time course of Statin effects * Time course established Days Years LDL-C lowered* Inflammation reduced Vulnerableplaques stabilized Endothelial function restored Ischemic episodes reduced Cardiac events reduced*
45. Lifestyle Modification approach in hypertension therapy 5–20 mm/10 kg wt loss Weight reduction All put together reduce BP by 20 to 55 mmHg 2–4 mmHg Abstinence from alcohol 4–9 mmHg Physical activity 2–8 mmHg Dietary sodium reduction 8–14 mmHg Adopt DASH [Dietary Approaches to Stop Hypertension] eating plan Approximate BP reduction [range] Modification
46.
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49. Hypertension Trial 42,418 high-risk hypertensive patients 90% previously treated, 10% untreated STEP 1 AGENTS Chlorthalidone 12.5-25 mg Amlodipine 2.5-10 mg Lisinopril 10-40 mg Doxazosin 1-8 mg N=15,255 N=9,048 N=9,054 N=9,061 STEP 2 AND 3 AGENTS (5 years)* Atenolol 28.0% Clonidine 10.6% Reserpine 4.3% Hydralazine 10.9% * Of participants with data available for determination. ALLHAT
54. Effect of various antihypertensives on coexisting disorders Parameter Diuretic ACEi, ARB β blocker Ca + Blocker Ischemia No effect Improves Improves Negative LVH, LVF Improves Improves Improves* Negative CV Mortality Improves Improves Improves Increases Heart rate No effect No effect Bradycardia Tachycardia Use in DM Negative Excellent Negative Negative Lipid effects Negative Excellent Negative Neutral Fluid & Na Enhances No effect Vasoconstr. Vasodilatory K ex / bronchi Enhances No effect Bronchospa No effect UA / Conduct. ↑ Uric acid No effect ↓ conduction No effect
56. Effect of various drugs on CHD risk Drugs 1995 14% – 25% Atenolol 19% Captopril 18% Enalapril 15-45% Doxazosin Effect on CHD risk Drug
57. Change in Lipid Levels with Doxazosin Treatment: HALT Study Total-C LDL-C Triglycerides HDL-C Change in Lipid Levels (mg/dl) Am Heart J 1996;131: 966-973
58. Changes in Lipid Parameters after 24 weeks Total Chol. HDL Chol. HDL Total Chol. Triglyc Am J Card 1987;59:103G Average ( + S.E.)
73. What is the essential approach in hypertension treatment?
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76.
Editor's Notes
The answer is C – 27 million. US Dept of Health and Human Services. JNC 7. The Seventh Report of the Joint National Committee on Prevention, Detection, Evaluation and Treatment of High Blood Pressure . Bethesda, Md: National Institutes of Health; May 2003. NIH Publication No. 03-5233. US Department of Health and Human Services (DHHS). National Center for Health Statistics. Third National Health and Nutrition Examination Survey, 1988-1994, NHANES III.
The answer is C – 27 million. US Dept of Health and Human Services. JNC 7. The Seventh Report of the Joint National Committee on Prevention, Detection, Evaluation and Treatment of High Blood Pressure . Bethesda, Md: National Institutes of Health; May 2003. NIH Publication No. 03-5233. US Department of Health and Human Services (DHHS). National Center for Health Statistics. Third National Health and Nutrition Examination Survey, 1988-1994, NHANES III.
The answer is B – 33%. According to analysis of data from the National Health and Nutrition Examination Survey, 1988-1994, approximately 27 million Americans have concomitant hypertension and dyslipidemia. Of those, only one third have been diagnosed with both conditions. US Department of Health and Human Services (DHHS). National Center for Health Statistics. Third National Health and Nutrition Examination Survey, 1988-1994, NHANES III.
The answer is A – 10%. Further, the same data show that only 3% are being treated to goal for both conditions.
Of the 10% of people treated for hypertension and dyslipidemia, only 3% get to goal.
Coupled with the findings from clinical trials, results from the M ultiple R isk F actor I ntervention T rial (MRFIT) offer strong support for intensified preventive efforts across all age groups. MRFIT found strong graded relationships between serum cholesterol levels above 180 mg/dL, systolic blood pressure (BP) >110 mm Hg, and diastolic BP >70 mm Hg and mortality due to coronary heart disease (CHD). Systolic BP was a stronger predictor than diastolic BP. Study Description: MRFIT was a randomized, multicenter primary prevention trial that studied the effect of intervention on the incidence of CHD. Between 1973 and 1975, more than 360,000 men aged 35 to 57 years in 18 US cities were screened for entry. Neaton JD, Wentworth D, for the Multiple Risk Factor Intervention Trial Research Group. Serum cholesterol, blood pressure, cigarette smoking, and death from coronary heart disease: overall findings and differences by age for 316 099 white men. Arch Intern Med . 1992;152:56-64.
The importance of systolic BP as a risk factor for coronary heart disease (CHD) is highlighted by the results of observational studies. An analysis of the 316,099 white men aged 35 to 57 screened between 1973 and 1975 for the Multiple Risk Factor Intervention Trial (MRFIT) assessed the influence of BP and other risk factors on death from CHD over a mean follow-up of 12 years. These men indicated that they had not been previously hospitalized for a heart attack or were not taking medication for diabetes. A strong risk gradient was evident for systolic BP for each category of diastolic BP category. Systolic BP was a stronger predictor of CHD death than was diastolic BP in all age groups. Neaton JD, Wentworth D, for the Multiple Risk Factor Intervention Trial Research Group. Serum cholesterol, blood pressure, cigarette smoking, and death from coronary heart disease: overall findings and differences by age for 316,099 white men. Arch Intern Med . 1992;152:56-64.
It is always a pleasure to present to ISHIB. My charge is to discuss the implications of the AASK trial on the management of hypertension in Blacks. The first implication is that we are beginning to accumulate data on the best way to lessen the toll that this disease extracts from our community.
The Pravastatin or Atorvastatin Evaluation and Infection Therapy–Thrombolysis in Myocardial Infarction 22 (PROVE IT–TIMI 22) trial demonstrated that in patients who have recently had an ACS, early and continued lowering of LDL-C to levels substantially below current target levels is of great benefit. Investigators compared 40 mg of pravastatin (standard therapy) daily with 80 mg of atorvastatin daily (intensive therapy) in 4162 patients who had been hospitalized for an ACS within the preceding 10 days The median LDL-C level achieved during treatment was 95 mg/dL in the standard-therapy group and 62 mg/dL in the intensive-therapy group ( P <0.001).
In the PROVE-IT trial, Kaplan-Meier estimates of the rates of the primary end point at 2 years were 26.3% and 22.4% for pravastatin and atorvastatin, respectively, indicating a 16% reduction in the hazard ratio in favor of atorvastatin ( P =0.005; 95% confidence interval, 5%-26%).
Potential time course of statin effects CHD risk reduction with a statin appears to occur as a result of several related changes, including restoration of endothelial function, reduction in inflammation, and stabilization of vulnerable plaque. The time course for these antiatherosclerotic effects of statins ranges from days to years. Within weeks to months after beginning statin therapy, endothelial function of coronary arteries is restored. Concurrent with this or following by just a few months is a reduction in inflammatory markers, such as high-sensitivity C-reactive protein. These effects appear to coincide with the reduction in ischemic events demonstrated after about 18 months of statin therapy. After several years of therapy (i.e., 1.5 – 2.5 years), fatal and nonfatal myocardial infarction rates begin to decline in statin-treated patients, and after 5 years of therapy, significant reductions have been documented. These changes coincide somewhat with stabilization of vulnerable atherosclerotic plaque during which the lipid-rich core of plaque is replaced with connective tissue and matrix.
Potential time course of statin effects CHD risk reduction with a statin appears to occur as a result of several related changes, including restoration of endothelial function, reduction in inflammation, and stabilization of vulnerable plaque. The time course for these antiatherosclerotic effects of statins ranges from days to years. Within weeks to months after beginning statin therapy, endothelial function of coronary arteries is restored. Concurrent with this or following by just a few months is a reduction in inflammatory markers, such as high-sensitivity C-reactive protein. These effects appear to coincide with the reduction in ischemic events demonstrated after about 18 months of statin therapy. After several years of therapy (i.e., 1.5 – 2.5 years), fatal and nonfatal myocardial infarction rates begin to decline in statin-treated patients, and after 5 years of therapy, significant reductions have been documented. These changes coincide somewhat with stabilization of vulnerable atherosclerotic plaque during which the lipid-rich core of plaque is replaced with connective tissue and matrix.
It is always a pleasure to present to ISHIB. My charge is to discuss the implications of the AASK trial on the management of hypertension in Blacks. The first implication is that we are beginning to accumulate data on the best way to lessen the toll that this disease extracts from our community.
DOES INCREASED IN GLUCOSE IN ALLHAT TRANSLATE INTO INCREASED RISK OF DM SEEN IN EPID STUDIES Points of Emphasis / Key Messages The risk of cardiovascular death is substantially increased in patients with type 2 diabetes and comorbid elevated SBP. For an SBP of 120 to 139 mm Hg, concurrent diabetes is equivalent to adding 40 mm Hg to the systolic pressure. In addition, MRFIT demonstrated that SBP (as well as elevated serum cholesterol levels and cigarette smoking) is a significant predictor of mortality in men with and without diabetes. The Multiple Risk Factor Intervention Trial (MRFIT) enrolled 361,662 men 35 to 37 years of age. A total of 5625 were receiving treatment for diabetes; the remaining 356,037 did not have diabetes. The study did not classify diabetes as insulin-dependent or non-insulin-dependent (NIDDM), but because of the participants’ age, more than 90% were assumed to have NIDDM. Men whose SBP was 180 mm Hg had nearly twice the risk of CV mortality if they had diabetes. If SBP was 140 to 179 mm Hg, the risk was more than twice that of men with diabetes. Reference Stamler J, Vaccaro O, Neaton JD, Wentworth D. Diabetes, other risk factors, and 12-yr cardiovascular mortality for men screened in the Multiple Risk Factor Intervention Trial. Diabetes Care . 1993;16:434-444.
This post-hoc comparison is of lisinopril (n=9054, 3210 Blacks) versus amlodipine (n=9048, 3213 Blacks).
It is always a pleasure to present to ISHIB. My charge is to discuss the implications of the AASK trial on the management of hypertension in Blacks. The first implication is that we are beginning to accumulate data on the best way to lessen the toll that this disease extracts from our community.
It is always a pleasure to present to ISHIB. My charge is to discuss the implications of the AASK trial on the management of hypertension in Blacks. The first implication is that we are beginning to accumulate data on the best way to lessen the toll that this disease extracts from our community.
Visceral adipose tissue is associated with a higher rate of free fatty acid (FFA) flux to the liver via the splanchnic circulation. In contrast, subcutaneous accumulation is not associated with direct effects in the liver, since FFA are released into the systemic circulation. FFA flux to the liver, in turn, is associated with a higher production of glucose, triglycerides, and VLDL; small, dense LDL particles, and lower HDL-C levels. Elevated FFA levels also inhibit glucose uptake by skeletal muscle, thereby contributing to impairment of insulin sensitivity, characteristic of the prediabetic state. Hyperinsulinemia, a result of reduced insulin sensitivity, enhances sodium reabsorption and increases sympathetic nervous system activity, resulting in elevated systolic blood pressure. Elevated FFA contribute to hypertension, dyslipidemia, and insulin resistance
It is always a pleasure to present to ISHIB. My charge is to discuss the implications of the AASK trial on the management of hypertension in Blacks. The first implication is that we are beginning to accumulate data on the best way to lessen the toll that this disease extracts from our community.
Thus, in the context of emerging evidence of vascular protection, the Goals of Therapy in hypertension need to be not only to control the BP, but also - To improve quality of life (symptoms) To reduce progression of CVD & induce regression, where possible and to reduce mortality & morbidity Thus, there is a change from the standard focus of controlling hypertension to a new, modified approach whereby in addition to BP control, there is the additional need to prevent the hypertension induced structural and functional abnormalities of the vascular endothelium. Correction of such endothelial dysfunction enables prevention of metabolic abnormalities and target organ damage and the restoration of the normal endothelium-dependent vasomotor tone. How can we achieve this? By adopting therapy that will restore the abnormal endothelium to a normal one. But, what is the difference between normal and abnormal endothelium?
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