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Query: UMLS:C0018801 (heart failure)
72,216 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Isolated systolic hypertension is the most common form of hypertension, especially among patients 50 years or older. What is not appreciated is that there are secondary causes of isolated systolic hypertension. Hyperthyroidism increases systolic blood pressure by decreasing systemic vascular resistance, increasing heart rate, and raising cardiac output. Potential cardiovascular consequences of hyperthyroidism include atrial arrhythmias (especially atrial fibrillation), pulmonary hypertension, left ventricular hypertrophy, and heart failure. The prevalence of hypertension is greater among hyperthyroid patients than euthyroid patients. Whether there is a blunted nocturnal decline in ambulatory blood pressure among hyperthyroid patients is more controversial. Treatment is associated with a reduction in systolic blood pressure, heart rate, and cardiac output.
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PMID:Hyperthyroidism: a secondary cause of isolated systolic hypertension. 1689 76

Heart failure (HF) affects approximately 5 million persons in the United States; more than 550,000 new cases of HF are reported each year. Prevalence of HF with a normal left ejection fraction increases with age and is higher in older women than older men. Both underlying and precipitating causes of HF should be treated when possible. Hypertension, especially isolated systolic hypertension, should be treated with diuretics, ACE inhibitors, and beta blockers. Myocardial ischemia should be treated with nitrates and beta blockers. Anemia should be treated, as should hyperthyroidism, hypothyroidism, and obstructive sleep apnea. Use of inappropriate drugs, such as nonsteroidal anti-inflammatory drugs, should be avoided. Coronary revascularization should be performed in selected individuals.
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PMID:Heart failure update: treatment of heart failure with a normal left ventricular ejection fraction in the elderly. 1690 Nov 93

Hypertension in elderly patients is common and is associated with unique challenges. This study examines the prevalence of comorbidities in elderly hypertensive patients and evaluates the association between comorbidities and other covariates with blood pressure goal attainment. Data were collected through retrospective review of medical records and included patient characteristics, comorbidities, treatment-related variables, and blood pressure goal attainment. At least 1 comorbidity was present in 88% of patients, and 61% had multiple comorbidities. The most common comorbidity was isolated systolic hypertension. The presence of diabetes or isolated systolic hypertension at initial visit and treatment with a thiazide diuretic at the final clinic visit were associated with significantly higher odds of patients not achieving blood pressure goal. A diagnosis of heart failure was associated with lower odds of not achieving blood pressure goal. These issues should be given special consideration during the evaluation, treatment selection, and long-term monitoring of this population.
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PMID:Prevalence of comorbidities and their influence on blood pressure goal attainment in geriatric patients. 1721 36

In myocardial ischaemia and heart failure, beta-blockers with intrinsic sympathomimetic activity (ISA) e.g. pindolol, xamoterol, bucindolol, nebivolol, have performed poorly in reducing morbidity and mortality. In both indications beta-1 blockade is the vital active ingredient. Beta-1 blockade (bisoprolol) is now an alternative first-line choice to Ace-inhibition in the treatment of heart failure. The therapeutic role of beta-blockers in hypertension is less well understood, particularly since the new recommendations in the UK from the NICE committee stating that: 1. beta-blockers are no longer preferred as a routine initial therapy, 2. the combination with diuretics is discouraged due to the risk of induced diabetes, and 3. in younger patients first-choice initial therapy should be an ACE-inhibitor. Recent data from the Framingham Heart Study and other epidemiological studies have indicated that the development of diastolic hypertension in younger subjects is closely linked to weight-increase and an increase in peripheral resistance; such subjects have a high adrenergic drive and cardiac output. In contrast, elderly systolic hypertension mostly arises de novo via poor vascular compliance. Thus in younger, probably overweight, hypertensives (including diabetics) first-line beta-blockade has performed well in preventing myocardial infarction (a fact hidden by meta-analyses that do not take age into account). Conversely, in elderly hypertensives first-line beta-blockade (atenolol) has performed poorly in reducing cardiovascular risk (due to partial beta-2 blockade atenolol evokes metabolic disturbance and does not improve vascular compliance, or effectively lower central aortic pressure or reverse left ventricular hypertrophy). Thus beta-blockers like atenolol are ill-equipped for first-line therapy in elderly hypertension. Some beta-blockers, e.g. bisoprolol (up to 10 mg/day is highly beta-1 selective) and nebivolol (beta-2/3 intrinsic sympathomimetic activity), do improve vascular compliance and cause no metabolic disturbance. Beta-blockers as second-line to low-dose diuretics (which, by improving vascular compliance and increasing sympathetic nerve activity, create an optimal environment for beta-blockade) in elderly hypertension (including diabetics) have performed well in reducing cardiovascular events (this combination has the added bonus of reducing the risk of bone fracture by about 30%). Meta-analyses which include studies where it is unclear whether a diuretic or beta-blocker was a first-line therapy will dilute the benefit stemming from first-line diuretic/second-line beta-blockade. Hypertensives (of all ages) with ischaemia are well suited to beta-blockade.
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PMID:Are we misunderstanding beta-blockers. 1743 71

Organic nitrates still constitute, like digitalis, an indispensable remedy. Amyl nitrite, discovered by Balard was the first to be used for the therapy of angina pectoris by Sir T. Lauder Brunton in 1867. Nitroglycerin (Glyceroltrinitrate) was synthetized by Ascanio Sobrero 1846 and was studied by Brunton, Tate, and Murrel who published his paper on the treatment of angina pectoris in 1879. It has been soon recognised that the main effect of nitrates is vasodilatation more pronounced in the veins, resulting in reduced venous return, decrease of left and right ventricular end-diastolic pressure and volume and in a reduction in the myocardioal oxygen demand. Sir William Osler was the first who suggested the use of nitroglycerin in patients with congestive heart failure "when the pulse is hard and firm", in his "Principles and Practice of Medicine" 1892. About fifty years later, L. Goldberg confirmed the antihypertensive effect of isosorbide dinitrate in a double--leticin trial on hypertensive patients. The long acting nitrates isosorbide dinitrate and isosorbide 5-mononitrate now share all the beneficial effects of nitroglycerin in patients with stable and unstable angina and in selected patients with heart failure. The sustained-release tablets of isosorbide 5-mononitrate have been shown to be effective with long-term use without inducing tolerance. The author also summaries basic data concerning the chemistry, pharmacology and clinical applications of organic nitrates and nitrocompounds. The position of nitrates in the treatment of isolated systolic hypertension in the elderly and of chronic heart failure is still to be established.
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PMID:[Milestones of cardiovascular therapy. III. Nitroglycerin]. 1765 May 92

The optimal hemoglobin level in patients with hypertension or heart failure is not yet defined. The aim of the present investigation was to examine the relation of hemoglobin with cardiovascular outcomes in high-risk patients with isolated systolic hypertension (ISH) and left ventricular hypertrophy (LVH). In 1,326 patients with ISH in the Losartan Intervention For Endpoint Reduction in Hypertension (LIFE) study, hemoglobin and cardiovascular outcomes were examined using Cox proportional hazard models. Baseline hemoglobin was negatively related to rate of cardiovascular death (hazard ratio 0.81 per 1 g/dl, 95% confidence interval [CI] 0.67 to 0.98, p = 0.032) after adjusting for baseline Framingham risk score, LVH, treatment, and estimated glomerular filtration rate. Hemoglobin decreased slightly during the study and the decrease was more pronounced in the losartan group (13.9 +/- 1.3 to 13.6 +/- 1.4 g/dl) than in the atenolol group (13.9 +/- 1.2 to 13.8 +/- 1.4 g/dl). Hemoglobin as a time-varying covariate was negatively associated with rate of cardiovascular death (hazard ratio 0.75, 95% CI 0.63 to 0.90, p <0.001) and stroke (hazard ratio 0.84, 95% CI 0.72 to 0.99, p = 0.040) after adjusting for baseline Framingham risk score, LVH, treatment, and estimated glomerular filtration rate. In conclusion, in this high-risk population with ISH and LVH, lower hemoglobin at baseline was associated with higher probability of cardiovascular death, and decrease in hemoglobin over time was associated with higher probability of cardiovascular death or stroke; this effect was attenuated by treatment with losartan.
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PMID:Effect of hemoglobin levels on cardiovascular outcomes in patients with isolated systolic hypertension and left ventricular hypertrophy (from the LIFE study). 1771 33

Cardiovascular disease remains the leading cause of death worldwide. The renin-angiotensin-aldosterone system (RAAS) plays a key role in the regulation of blood pressure, through the actions of angiotensin (Ang) II. Excessive RAAS activity may lead to hypertension and associated target organ damage. Indeed, RAAS blockade with angiotensin converting enzyme inhibitors (ACEIs) and/or angiotensin receptor AT (1) blockers (ARBs) has proved to be successful treatment for arterial hypertension, heart failure and diabetes. Accumulating evidence suggests that arterial stiffness is an important and independent predictor of cardiovascular risk. More recently, a role for advanced glycation end-products (AGEs) in the development of arterial stiffening has been suggested. Advanced glycation end-products form by a nonenzymatic reaction between reducing sugars and biological proteins. Mechanisms underlying these alterations include AGE cross-linking of collagen and AGE interactions with circulating proteins and AGE receptors. New pharmacologic agents that prevent AGE formation, break cross-links, or block AGE receptors reduce vascular and myocardial stiffness, inhibit atherosclerotic plaque formation, and improve endothelial function. These agents promise to reduce the risk of isolated systolic hypertension, diastolic dysfunction, diabetes and thus, heart failure.
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PMID:Inhibition of renin-angiotensin system and advanced glycation end products formation: a promising therapeutic approach targeting on cardiovascular diseases. 1797 87

Exercise training improves functional capacity and quality of life in patients with heart failure. However, the long-term effects of exercise on mortality associated with hypertensive heart disease have not been well defined. In the present study, we investigated the effect of low-intensity exercise training on disease progression and survival in female spontaneously hypertensive heart failure rats. Animals with severe hypertension (16 months old) were treadmill trained (14.5 m/min, 45 min/d, 3 d/wk) until they developed terminal heart failure or were euthanized because of age-related complications. Exercise delayed mortality resulting from heart failure (P<0.001) and all causes (P<0.05) and transiently attenuated the systolic hypertension and contractile dysfunction observed in the sedentary animals but had no effect on cardiac morphology or contractile function in end-stage heart failure. Training had no effect on terminal myocardial protein expression of antioxidant enzymes, calcium handling proteins, or myosin heavy chain isoforms but was associated with higher cytochrome oxidase activity in cardiac mitochondria (P<0.05) and a greater mitochondrial content of cardiolipin, a phospholipid that is essential for optimal mitochondrial energy metabolism. In conclusion, low-intensity exercise training significantly delays the onset of heart failure and improves survival in female hypertensive heart failure rats without eliciting sustained improvements in blood pressure, cardiac function, or expression of several myocardial proteins associated with the cardiovascular benefits of exercise. The effects of exercise on cytochrome oxidase and cardiolipin provide novel evidence that training may improve prognosis in hypertensive heart disease by preserving mitochondrial energy metabolism.
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PMID:Low-intensity exercise training delays heart failure and improves survival in female hypertensive heart failure rats. 1825 16

Cerebrovascular disease is a major cause of morbidity and mortality worldwide and its prevalence is expected to increase as a result of projected demographic trends. Stroke is one of the leading causes of disability and death of over 30 million people each year worldwide. Hypertension is the most important modifiable risk factor for stroke. Recent data indicate that treatment with antihypertensive drugs reduces the incidence of all strokes in men (by 34%), women (by 38%), the elderly (by 36%), including those older than 80 years (by 34%), younger persons, those with systolic and diastolic hypertension, persons with isolated systolic hypertension, and those with a history of stroke or transient ischemic attack (by 28%). Furthermore, several large, prospective, randomized, clinical outcome trials have shown that calcium channel blockers (CCBs) are effective and safe antihypertensive drugs compared with placebo and reduce the cardiovascular morbidity and mortality of treated patients. Moreover, when CCBs were compared with conventional antihypertensive drugs they demonstrated similar blood pressure-lowering effects and similar reductions in cardiovascular morbidity and mortality, with the exception of a higher incidence of heart failure and fatal myocardial infarction in some studies. Considering all the evidence available today, however, these drugs should be considered safe for the treatment of the uncomplicated hypertensive patient in combination with other drugs. They can also be used as first-line therapy for older, stroke-prone hypertensive patients. The aim of this review is to summarize the role of CCBs in the prevention of stroke.
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PMID:Aggressive blood pressure control and stroke prevention: role of calcium channel blockers. 1839 22

In healthy subjects the arterial system and the left ventricle (LV) are tightly coupled at rest to optimize cardiac performance. Systolic hypertension (SH) is a major risk factor for heart failure and is associated with structural and functional alterations in the arteries and the LV. The effects of SH and resting systolic blood pressure (SBP) on arterial-ventricular coupling (E(a)I/E(LV)I) at rest, at peak exercise, and during recovery are not well described. We noninvasively characterized E(a)I/E(LV)I as end-systolic volume index/stroke volume index in subjects who were normotensive (NT, n = 203) or had SH (brachial SBP > or =140 mmHg, n = 79). Cardiac volumes were measured at rest and throughout exhaustive upright cycle exercise with gated blood pool scans. E(a)I/E(LV)I reserve was calculated by subtracting peak from resting E(a)I/E(LV)I. At rest, E(a)I/E(LV)I did not differ between SH and NT men but was 23% (P = 0.001) lower in SH vs. NT women. E(a)I/E(LV)I did not differ between SH and NT men or women at peak exercise or during recovery. Nevertheless, E(a)I/E(LV)I reserve was 61% (P < 0.001) lower in SH vs. NT women. Similarly, resting SBP (as a continuous variable) was not associated with E(a)I/E(LV)I in men (beta = -0.12, P = 0.17) but was inversely associated with E(a)I/E(LV)I in women (beta = -0.47, P < 0.001). SH and a higher resting brachial SBP are associated with a lower E(a)I/E(LV)I at rest in women but not in men, and SH women have an attenuated E(a)I/E(LV)I reserve. Whether a smaller E(a)I/E(LV)I reserve leads to functional limitations warrants further examination.
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PMID:The sex-specific impact of systolic hypertension and systolic blood pressure on arterial-ventricular coupling at rest and during exercise. 1845 31


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