Management of Hypertension among Patients with Coronary Heart Disease

Evidence suggests that coronary heart disease (CHD) is the most common outcome of hypertension. Hypertension accelerates the development of atherosclerosis, and sustained elevation of blood pressure (BP) can destabilize vascular lesions and precipitate acute coronary events. Hypertension can cause myocardial ischemia in the absence of CHD. These cardiovascular risks attributed to hypertension can be reduced by optimal BP control. Although several antihypertensive agents exist, the choice of agent and the appropriate target BP for patients with CHD remain controversial. In this succinct paper, we examine the evidence and the mechanisms for the linkage between hypertension and CHD and we discuss the treatment options and the goals of therapy that are consistent with the report of the seventh Joint National Committee on the Prevention, Detection, Evaluation, and Treatment of High Blood Pressure (JNC 7) and American Heart Association scientific statement. We anticipate changes in the recommendations of the forthcoming JNC 8

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Evidence suggests that coronary heart disease (CHD) is the most common outcome of hypertension. Hypertension accelerates the development of atherosclerosis, and sustained elevation of blood pressure (BP) can destabilize vascular lesions and precipitate acute coronary events. Hypertension can cause myocardial ischemia in the absence of CHD. These cardiovascular risks attributed to hypertension can be reduced by optimal BP control. Although several antihypertensive agents exist, the choice of agent and the appropriate target BP for patients with CHD remain controversial. In this succinct paper, we examine the evidence and the mechanisms for the linkage between hypertension and CHD and we discuss the treatment options and the goals of therapy that are consistent with the report of the seventh Joint National Committee on the Prevention, Detection, Evaluation, and Treatment of High Blood Pressure (JNC 7) and American Heart Association scientific statement. We anticipate changes in the recommendations of the forthcoming JNC 8. Background Hypertension is not only a major risk factor for stroke and heart failure (HF), but more importantly for coronary heart disease (CHD). Based on the blood pressure (BP) cutoff of ≥140/90 mm Hg for hypertension, as defined by the seventh report of the Joint National Committee on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure (JNC 7) Hypertension accelerates the development and progression of atherosclerosis, and sustained elevation of BP can destabilize vascular lesions and precipitate acute coronary events. Hypertension by itself can cause myocardial ischemia in the absence of CHD. These CVS risks attributed to hypertension can be greatly reduced by optimal control of BP. Although several antihypertensive agents exist, the optimal choice of agents and the appropriate target BP for patients with CHD remain controversial. The goals of 2 International Journal of Hypertension treating patients with hypertension and CHD are to lower BP, reduce ischemia, and prevent CVS events. In this succinct paper, we examine the epidemiological evidence and the pathophysiological mechanisms for the linkage between hypertension and CHD and we discuss the treatment options and the goals of therapy that are consistent with the recommendations of JNC 7 and American Heart Association (AHA) scientific statement Link between Hypertension and Coronary Heart Disease The pathophysiological link between hypertension and CHD can be described under two major pathways as described below and shown in Atherogenesis. The physical impact of high BP can cause endothelial injury. Injured endothelium results in impairment in the synthesis and the release of the potent vasodilator-nitric oxide and also promotes the accumulation of reactive oxygen species and other inflammatory factors which mediate the development of atherosclerosis, thrombosis, and vascular occlusion. This inflammatory process is a prominent feature in the pathogenesis of both hypertension and atherosclerosis Increased Afterload and Left Ventricular Hypertrophy. Hypertension by itself can cause myocardial ischemia in the absence of CHD. Increased afterload due to hypertension can result in significant left ventricular hypertrophy (LVH), which may impair ventricular relaxation and compromise coronary blood flow during diastole. Although genetic factors have been associated with LVH, chronic uncontrolled hypertension appears to be the major cause Research has shown that LVH diminishes coronary flow reserve Therapy for Hypertension in CHD Both JNC 7 and 2007 AHA guideline stressed the importance of antihypertensive therapy in the high-risk population, including CHD β-blockers are heterogenous class of agents with differing pharmacological effects. The cardioselective β-blockers without intrinsic sympathomimetic activity are generally preferred. These agents reduce myocardial oxygen consumption and heart rate and enhance coronary flow by increasing diastolic filling period. Among patients with both acute myocardial infarction (MI) and hypertension, β-Blockers have been shown to limit infarct size, improve survival, and decrease the risk of recurrent MI and the incidence of sudden cardiac death, which is secondary to fatal arrhythmias Calcium Channel Blockers. Long-acting dihydropyridines calcium channel blockers (CCBs), amlodipine, and nifedipine can be added to the basic regimen if BP remains elevated or angina continues while on β-blocker therapy. The nondihydropyridine agents, diltiazem and verapamil, can also be substituted for β-blocker when contraindications exist or side effects develop They also increase myocardial O 2 supply by dilating coronary arteries. Several large randomized trials have evaluated the use of CCBs in hypertension control. The Controlled-Onset Verapamil IN Cardiovascular Endpoint (CONVINCE) trial, the NORdic DILtiazem (NORDIL) study, and the International VErapamil SR/Trandolapril (INVEST) study showed that outcomes with CCBs-based therapy were not different from those of β-blockers-based therapy Nitrates. Nitrates have not been shown to be of significant use in hypertension treatment; however, they are indicated for acute relief of angina or treatment of chronic angina which cannot be controlled with β-blockers and CCBs. The reports of two large trials comparing nitrates with placebo showed no difference in mortality with the use of nitrates 3.6. Angiotensin-Converting Enzyme. ACE inhibitors are recommended for use in all patients after MI. Two major trials, the European Trial on Reduction of Cardiac Events with Perindopril in Stable Coronary Artery Disease (EUROPA) and Heart Outcome Prevention Evaluation (HOPE) study, showed the cardioprotective effect of ACE inhibitor in hypertensive CHD patients 3.7. Angiotensin-Receptor Blockers. In individuals who are ACE inhibitor intolerant or allergic, angiotensin receptors blockers (ARBs) have been shown to be an effective alternative in the treatment of hypertension, CHD, and HF. Emerging data appear to support the use of ARBs in MI. In the VALIANT study, the ARB, valsartan was as effective as captopril in patients at high risk of CVS events after MI 3.8. Diuretic. The ALLHAT trial clearly showed the benefit of thiazide diuretic in the treatment of hypertension Combination and Adjunctive Therapy. The control of BP is more important than the choice of antihypertensive agent in the prevention CHD and other complications of hypertension Conclusion The target BP in hypertensive patients with CHD is <130/80 mm Hg with caution in lowering the DBP below 60 mm Hg. To achieve this target, effective combination antihypertensive drug therapy is usually required to achieve and sustain long-term BP control. Treatment regimen should include β-blocker, ACE inhibitor, or ARB, most especially if there is LV systolic dysfunction and/or diabetes mellitus, and possibly a thiazide diuretic. CCBs can be used as alternative to β-blocker or added to the basic regimen, and nitrates are useful for relieve of ischemic pain. The overall goal of therapy is to reduce morbidity and mortality associated with both hypertension and CHD. As more data from hypertension trials are made available, we anticipate changes in the recommendations of the forthcoming JNC 8

Functional capacity is a better predictor of coronary heart disease than depression or abnormal sleep duration in Black and White Americans

To assess whether functional capacity is a better predictor of coronary heart disease (CHD) than depression or abnormal sleep duration. Adult civilians in the USA (n=29,818, mean age 48±18years, range 18–85years) were recruited by a cross-sectional household interview survey using multistage area probability sampling. Data on chronic conditions, estimated habitual sleep duration, functional capacity, depressed moods, and sociodemographic characteristics were obtained. Thirty-five percent of participants reported reduced functional capacity. The CHD rates among White and Black Americans were 5.2% and 4%, respectively. Individuals with CHD were more likely to report extreme sleep durations (short sleep [⩽5h] or long sleep [⩾9h]; odds ratio [OR] 1.65, 95% confidence interval [CI] 1.38–1.97; P<0.0001), less likely to be functionally active (anchored by the ability to walk one-quarter of a mile without assistance [OR 6.27, 95% CI 5.64–6.98; P<0.0001]) and more likely to be depressed (OR 1.78, 95% CI 1.60–1.99; P<0.0001) than their counterparts. On multivariate regression analysis adjusting for sociodemographic factors and health characteristics, only functional capacity remained an independent predictor of CHD (OR 1.81, 95% CI 1.42–2.31; P<0.0001). Functional capacity was an independent predictor of CHD in the study population, whereas depression and sleep duration were not independent predictors

Sleep Duration and Reported Functional Capacity among Black and White US Adults

Objective: Evidence suggests that individuals reporting sleeping below or above the population's modal sleep duration are at risk for diabetes, hypertension, and other cardiovascular diseases. Evidence also indicates that individuals with these conditions have reduced functional capacity. We assessed whether reported sleep duration and functional capacity are independently associated and whether individuals' race/ethnicity has an effect on this association. Method: Data were obtained from 29,818 black and white Americans (age range: 18-85 years) who participated in the 2005 National Health Interview Survey (NHIS). The NHIS uses a multistage area probability design sampling of non-institutionalized representatives of the US civilian population. Of the sample, 85% were white and 56% were women. Results: Univariate logistic regression analysis showed that individuals sleeping 8 h were 3.77 times more likely to be functionally impaired (36% vs 13%; p < 0.001). Individuals of the black race/ethnicity were more likely to be functionally impaired than their white counterparts (23% vs 19%; p < 0.001). Multivariate-adjusted regression analyses showed significant interactions between individuals' race/ethnicity and short sleep with respect to functional capacity (black: OR = 2.78, p < 0.0001; white: OR = 2.30, p < 0.0001). Significant interactions between race/ethnicity and long sleep were also observed (black: OR = 2.43, p < 0.001; white: OR = 2.63, p < 0.001). Conclusion: Our findings suggest that individuals' habitual sleep duration and their race/ethnicity are significant predictors of their functional capacity

Functional capacity is a better predictor of coronary heart disease than depression or abnormal sleep duration in Black and White Americans

OBJECTIVE: To assess whether functional capacity is a better predictor of coronary heart disease (CHD) than depression or abnormal sleep duration. METHODS: Adult civilians in the USA (n=29,818, mean age 48 ± 18 years, range 18–85 years) were recruited by a cross-sectional household interview survey using multistage area probability sampling. Data on chronic conditions, estimated habitual sleep duration, functional capacity, depressed moods and sociodemographic characteristics were obtained. RESULTS: Thirty-five percent of participants reported reduced functional capacity. The CHD rates among White and Black Americans were 5.2% and 4%, respectively. Individuals with CHD were more likely to report extreme sleep durations [short sleep (≤ 5 h) or long sleep (≥ 9 h); odds ratio (OR) 1.65, 95% confidence interval (CI) 1.38–1.97; P<0.0001], less likely to be functionally active [anchored by the ability to walk one-quarter of a mile without assistance (OR 6.27, 95% CI 5.64–6.98; P<0.0001)] and more likely to be depressed (OR 1.78, 95% CI 1.60–1.99; P<0.0001) than their counterparts. On multivariate regression analysis adjusting for sociodemographic factors and health characteristics, only functional capacity remained an independent predictor of CHD (OR 1.81, 95% CI 1.42–2.31; P<0.0001). CONCLUSION: Functional capacity was an independent predictor of CHD in the study population, whereas depression and sleep duration were not independent predictors

Sleep insufficiency and the natural environment: Results from the US Behavioral Risk Factor Surveillance System survey

BACKGROUND: Exposure to the natural environment may improve health behaviors and mental health outcomes such as increased levels of physical activity and lower levels of depression associated with sleep quality. Little is known about the relationship between insufficient sleep and the natural environment. PURPOSE: To determine whether exposure to attributes of the natural environment (e.g., greenspace) attenuates the likelihood of reporting insufficient sleep among US adults. METHODS: Multiple logistic regression models were used to explore the association between self-reported days of insufficient sleep (in the past 30 days) and access to the natural environment in a multi-ethnic, nationally representative sample (n=255,171) of US adults ≥18 years of age enrolled in the 2010 Behavioral Risk Factor Surveillance System. RESULTS: Using 1-to-6 days of insufficient sleep as the referent group for all analyses, lower odds of exposure to natural amenities were observed for individuals reporting 21-to-29 days (OR=0.843, 95% Confidence Interval (CI) = 0.747, 0.951) of insufficient sleep. In stratified analyses, statistically significant lower odds of exposure to natural amenities was found among men reporting7-to-13-days (OR = 0.911, 95% CI = 0.857, 0.968), 21-to-29-days (OR=0.838, 95% CI=0.759, 0.924), and 30-days (OR=0.860, 95%CI=0.784, 0.943) of insufficient sleep. Greenspace access was also protective against insufficient sleep for men and individuals aged 65+. CONCLUSIONS: In a representative sample of US adults, access to the natural environment attenuated the likelihood of reporting insufficient sleep, particularly among men. Additional studies are needed to examine the impact of natural environment exposure on sleep insufficiency across various socio-demographic groups