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Query: UMLS:C0018799 (heart disease)
34,133 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Hypertension, a major risk factor for cerebrovascular disease and heart disease, often requires drug therapy. The First Japanese Society of Hypertension Guidelines for the Management of Hypertension were published in June 2000. In the present work, we surveyed 447 doctors who attended continuing medical education meetings between March and July 2001 to elucidate national antihypertensive treatment patterns. A minimum level of 150/95 mmHg was selected by 60% and 140/90 mmHg by 19% of respondents as thresholds for initiating drug treatment, while 130/85 mmHg was selected by 26% of respondents as the goal blood pressure in middle-aged uncomplicated male patients. Sixty-nine percent of respondents selected a calcium antagonist as their previous drug of the first choice and 22% selected an ACE inhibitor. For their future first choice, 55% would prescribe an angiotensin II receptor antagonist (AIIA); 19% an ACE inhibitor; and 16% a calcium antagonist. Seventy-two percent selected a calcium antagonist + an ACE inhibitor and 17% selected a calcium antagonist + AIIA as their previous first-choice drug combinations. For their future drug combinations, 56% would select an AIIA + a calcium antagonist and 25% a calcium antagonist + an ACE inhibitor. Four weeks or less was selected by 69% of respondents as the period intended to reach the goal blood pressure. Eight weeks or more was selected by 28%. Overall, our data suggest that doctors in Japan are still cautious and conservative in controlling blood pressure levels but want rapid achievement of the goal blood pressure. Their first choice drug is shifting from calcium antagonists to AIIAs. These findings indicate the need for continued effort to evaluate the diversity of clinical practice and assess the appropriateness of continuing medical education.
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PMID:Trends in pharmacologic management of hypertension in Japan one year after the publication of the JSH 2000 guidelines. First Japanese Society of Hypertension. 1204 31

The elderly population is expanding rapidly throughout the world. Hypertension, heart disease and other cardiovascular disorders are prevalent conditions among this age group. Consequently, clinicians will spend a large proportion of their practices managing older adults with cardiovascular disorders. A large proportion of this time will be devoted to using pharmacotherapeutic strategies for the long-term management of chronic conditions. The physiological changes that accompany aging affect cardiovascular function, and the pharmacokinetics and pharmacodynamics of many cardiovascular medications are altered by these physiological changes. The interactions of these changes can have a profound effect on the agents used to treat cardiovascular disorders and may alter their therapeutic outcomes. Several classes of medications are used to treat chronic cardiovascular disorders in older adults. These include the ACE inhibitors and angiotensin II receptor antagonists, calcium channel antagonists, beta-adrenoceptor antagonists (beta-blockers), oral antiarrhythmic agents and warfarin. Drugs such as beta-blockers may aggravate decreased cardiac output and increase peripheral resistance, but are valuable adjuncts in many patients with congestive heart failure. Agents that reduce angiotensin II activity may have several benefits for treating heart failure and hypertension. Successful treatment of cardiovascular disorders in older adults requires the choice of the most appropriate agent, taking into consideration the complex interactions of pharmacokinetics, pharmacodynamics and disease effects.
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PMID:Cardiovascular drug therapy in the elderly: theoretical and practical considerations. 1271 Aug 64

Advanced heart failure, also be defined as stage D heart failure, characterized by advanced structural heart disease and marked symptoms of heart failure at rest despite dietary modification, salt restriction and maximal medical therapy including ACE inhibitors, angiotensin II receptor blockers, digitalics, diuretics and beta blockers. These patients require frequent hospitalizations and specialized interventions such as heart transplantation, implantation of mechanical assistance devices, continuous intravenous inotropic therapy to palliate symptoms, or continued terminal care.
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PMID:[Management of advanced or refractory heart failure]. 1568 Jan 39

The primary aim of this study was evaluation of the efficacy of telmisartan (angiotensin II receptor blocker- AT(1) blocker) on blood pressure in 10 patients with renal impairment in moderate or advanced stages of renal insufficiency and not dependent on haemodialysis. Its effect on proteinuria, renal function (represented by serum urea, creatinine, glomerular filtration), evaluation of overall therapy compliance in comparison with a previously prescribed angiotensin converting enzyme inhibitors (ACEI) were secondary aims. Considering the presence of left ventricle hypertrophy in all patients as a marker of hypertensive cardiopathy, the effect of telmisartan therapy on non-invasive cardiovascular parameters (ECG, echocardiography, and assessment of heart rate variability-HRV) was also evaluated. The study group involved 10 hypertensive patients (6 women, 4 men) with diabetic and non-diabetic renal impairment, proteinuria above 1 g/24 hours, hypertensive cardiopathy and intolerance of ACEI (cough). Telmisartan was added to their long-term antihypertensive combination therapy in a dose of 40 mg for the first 14 days, after which the dose increased to the maximal of 80 mg. The average initial daytime systolic blood pressure (SBP) was 149 +/- 19.7 mm Hg, average night-time SBP 145 +/- 23.0 mm Hg, average initial daytime diastolic BP (DBP) 90.6 +/- 2.5 mm Hg, night-time DBP 88.9 +/- 13.5 mm Hg. Average initial serum creatinine was 207.2 +/- 48.5 micromol/l, urea 15.1 +/- 4.4 mmol/l, GF 0.5 +/- 0.1 ml/s. Echocardiography revealed left ventricular (LV) hypertrophy with well preserved systolic and moderately impaired diastolic LV function. Also the HRV assessment revealed impaired neurovegetative (e.g. sympathovagal) balance. After 1 year of combination therapy with telmisartan, there was a clearly significant reduction in both SBP and DBP in both day and night-time (SBP daytime 149.6 vs.116.6 mm Hg, night-time 145.8 vs. 129.5 mm Hg; DBP daytime 90.6 vs. 83.5 mm Hg, night-time 88.9 vs. 79.3 mm Hg) and proteinuria (2.37 vs. 1.27 g/24 hour, p < 0.05). There were no significant changes in serum creatinine, urea values, and LV functions. On the other hand, further progression of the sympathovagal balance impairment was noted (continuing reduction of HRV in 9 from 10 patients), which can be described as the priority finding. The total compliance of telmisartan therapy was very good and without adverse clinical side effects. In conclusion - telmisartan reduces blood pressure and proteinuria safely and effectively in patients with various types of nephropathy in moderate or advanced stages of renal insufficiency.
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PMID:Telmisartan in the treatment of hypertension in patients with chronic renal insufficiency. 1552 50

A progressive chain of pathophysiological events links cardiovascular risk factors to clinical manifestations of disease and life-threatening cardiovascular events. This chain--the cardiovascular continuum--underlies cardiovascular disease and holds the key to its prevention and treatment. Progressive tissue damage can result in morbidity from congestive heart failure, end-stage heart disease, nephrotic proteinuria and dementia and, eventually, death from cardio- or cerebrovascular causes. The renin-angiotensin-aldosterone system (RAAS) is involved at all stages of the cardiovascular continuum, because the effector molecules of the RAAS, angiotensin II in particular, have direct pathobiological effects on a variety of tissues, including the endothelium, vascular smooth muscle and the renal mesangium. Clinical trials of angiotensin II receptor blockers (ARBs) and angiotensin-converting enzyme (ACE) inhibitors have demonstrated the essential validity of this hypothesis. Interruption of the RAAS has been shown to reduce cardiovascular morbidity and mortality in patients with left ventricular hypertrophy, heart failure and post-myocardial infarction, as well as renal disease in patients with type 2 diabetes. Key questions remain, however. What are the clinical effects of combination ARB and ACE inhibitor treatment? How will combinations of RAAS blockade with other agents, such as statins, affect the cardiovascular continuum? Answers to these questions will require well-planned, adequately powered clinical trials, such as the Programme of Research tO evaluate Telmisartan End-organ proteCTION (PROTECTION) and the ONgoing Telmisartan Alone and in combination with Ramipril Global Endpoint Trial (ONTARGET) programmes. However, it is already clear that RAAS blockade is an essential part of blocking progression along the cardiovascular continuum.
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PMID:The cardiovascular continuum and renin-angiotensin-aldosterone system blockade. 1582 52

The incidence of diabetes is increasing at an alarming rate to the point where it is becoming an epidemic. An ageing population, sedentary lifestyle and an unhealthy diet are considered to have contributed toward this. What we must now consider is not only the burden of the disease but the complications that arise from diabetes, in particular kidney and heart disease. Foremost, more than half of the diabetic population will die from cardiovascular-related causes. Whilst diabetes is most often associated with hypertension, dyslipidaemia and obesity, these factors do not fully account for the increased burden of cardiovascular disease in people with diabetes. This strengthens the need for comprehensive studies investigating the underlying mechanisms mediating diabetic cardiovascular disease, and more specifically, diabetes-associated atherosclerosis. In addition to the recognised metabolic abnormalities associated with diabetes, upregulation of putative pathological pathways such as advanced glycation endproducts, renin-angiotensin system, oxidative stress and increased expression of growth factors and cytokines have been observed in the setting of diabetes. All of these have been shown to play a causal role in atherosclerotic plaque formation and thus may explain the increased risk of macrovascular complications in those patients with diabetes. In this review the effect of inhibiting the renin-angiotensin system with angiotensin converting enzyme inhibition and a comparison to angiotensin II receptor antagonism is discussed, with the results of clinical trails reflecting the more recently discovered, non-haemodynamic, proatherogenic actions of angiotensin II. The need for experimental models of diabetes-associated atherosclerosis will be covered, with particular emphasis given to the streptozotocin-diabetic apolipoprotein E knockout mouse. Finally, growth factors, including vascular endothelial growth factor and platelet-derived growth factor are discussed in detail.
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PMID:Preventing atherosclerosis with angiotensin-converting enzyme inhibitors: emphasis on diabetic atherosclerosis. 1650 70

The effect of diabetes on sarcolemmal Na(+)-K(+) pump function is important for our understanding of heart disease associated with diabetes and design of its treatment. We induced diabetes characterized by hyperglycemia but no other major metabolic disturbances in rabbits. Ventricular myocytes isolated from diabetic rabbits and controls were voltage clamped and internally perfused with the whole cell patch-clamp technique. Electrogenic Na(+)-K(+) pump current (I(p), arising from the 3:2 Na(+)-to-K(+) exchange ratio) was identified as the shift in holding current induced by Na(+)-K(+) pump blockade with 100 micromol/l ouabain in most experiments. There was no effect of diabetes on I(p) recorded when myocytes were perfused with pipette solutions containing 80 mmol/l Na(+) to nearly saturate intracellular Na(+)-K(+) pump sites. However, diabetes was associated with a significant decrease in I(p) measured when pipette solutions contained 10 mmol/l Na(+). The decrease was independent of membrane voltage but dependent on the intracellular concentration of K(+). There was no effect of diabetes on the sensitivity of I(p) to extracellular K(+). Pump inhibition was abolished by restoration of euglycemia or by in vivo angiotensin II receptor blockade with losartan. We conclude that diabetes induces sarcolemmal Na(+)-K(+) pump inhibition that can be reversed with pharmacological intervention.
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PMID:Alloxan-induced diabetes reduces sarcolemmal Na+-K+ pump function in rabbit ventricular myocytes. 1702 Sep 34

Heart disease and stroke are the most life-threatening consequences of diabetes mellitus, with mortality rates up to two to four times higher for persons with diabetes vs. those without and accounting for up to 65% of deaths. The cardiometabolic syndrome is a potent indicator of future risk of type 2 diabetes and concomitant increased potential for cardiovascular morbidity and mortality. Pharmacologic treatment is usually necessary to improve blood pressure and lipids, thereby decreasing the risk of cardiovascular disease. The reduction of cardiovascular and renal risk with type 2 diabetes and elevated blood pressure are compelling indications for thiazide diuretics, blockers, angiotensin-converting enzyme inhibitors, angiotensin II receptor blockers, and calcium channel blockers. Nevertheless, most patients with type 2 diabetes and elevated blood pressure will require two or more agents to lower blood pressure to the recommended goal of <130/80 mm Hg, and combination therapy may be beneficial. In patients with the cardiometabolic syndrome without type 2 diabetes, the present goal is to maintain BP <140/90 mm Hg, although recent data suggest potential decrease in the progression of prehypertension to hypertension with antihypertensive medication. Furthermore, blockers of the renin-angiotensin system may actually prevent newonset diabetes. It is reasonable for patients with type 2 diabetes and cardiovascular disease to achieve an optional low-density lipoprotein cholesterol (LDL-C) goal <70 mg/dL, and statin therapy should be considered regardless of baseline LDL-C level. In patients with the cardiometabolic syndrome without type 2 diabetes and calculated moderately high-risk status (two or more risk factors; 10-year risk, 10%-20%), the present goal for LDL-C is <130 mg/dL, with perhaps a therapeutic option of <100 mg/dL, and in patients with the cardiometabolic syndrome at lower risk, the LDL-C goal remains <160 mg/dL. Multifactorial management must be utilized to prevent progression of cardiovascular risk with the cardiometabolic syndrome and the ravages of cardiovascular disease in persons with type 2 diabetes, including antiplatelet therapy with aspirin.
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PMID:Management of cardiovascular risk in patients with type 2 diabetes mellitus as a component of the cardiometabolic syndrome. 1767 32

Inhibition of renin-angiotensin system (RAS) activity using angiotensin-converting enzyme inhibitors or angiotensin II receptor blockers (ARBs) is beneficial in patient populations with left ventricular dysfunction or systolic heart failure (HF) and other forms of heart disease. In high-risk patients with coronary heart disease (CHD), treatment with these agents reduces the mortality rate and improves secondary outcomes. Individuals with stable CHD who are at lower risk benefit less from treatment. RAS inhibition also provides some clinical benefit to patients with diastolic HF and preserved left ventricular function. Left ventricular hypertrophy (LVH) is a strong predictor of cardiovascular events and all-cause mortality in patients with hypertension. Treatment with an ARB reduces the risk for adverse cardiovascular outcomes in patients with hypertension and LVH. The benefits correlate with regression of LVH, and the effect is independent of the degree of blood pressure lowering. Finally, studies indicate that a history of hypertension in patients who have not had a myocardial infarction (MI) increases the risk for HF after MI; the risk is decreased in patients with hypertension who receive treatment with a RAS inhibitor.
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PMID:Management of hypertension in patients with cardiac disease: use of renin-angiotensin blocking agents. 1863 17

The steroid hormone aldosterone regulates sodium and potassium homeostasis. Aldosterone and activation of the mineralocorticoid receptor also causes inflammation and fibrosis of the heart, fibrosis and remodelling of blood vessels and tubulointerstitial fibrosis and glomerular injury in the kidney. Aldosterone and mineralocorticoid-receptor activation initiate an inflammatory response by increasing the generation of reactive oxygen species by nicotinamide adenine dinucleotide phosphate (NADPH) oxidase and mitochondria. High salt intake potentiates these effects, in part by activating the Rho family member Rac1, a regulatory subunit of reduced NADPH oxidase that activates the mineralocorticoid receptor. Studies in mice in which the mineralocorticoid receptor has been deleted from specific cell types suggest a key role for macrophages in promoting inflammation and fibrosis. Aldosterone can exert mineralocorticoid-receptor-independent effects via the angiotensin II receptor and via G-protein-coupled receptor 30. Mineralocorticoid-receptor antagonists are associated with decreased mortality in patients with heart disease and show promise in patients with kidney injury, but can elevate serum potassium concentration. Studies in rodents genetically deficient in aldosterone synthase or treated with a pharmacological aldosterone-synthase inhibitor are providing insight into the relative contribution of aldosterone compared with the contribution of mineralocorticoid-receptor activation in inflammation, fibrosis, and injury. Aldosterone-synthase inhibitors are under development in humans.
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PMID:Contribution of aldosterone to cardiovascular and renal inflammation and fibrosis. 2377 12


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