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The HOPE TIPS study assessed the practicality and tolerability of ramipril titration to a target dose of 10 mg (as achieved in definitive efficacy studies) in a clinical practice setting. 3881 patients at high cardiovascular risk (HOPE study criteria) were recruited in primary and specialist care settings in 9 countries by 439 investigators. Dose titration of ramipril from 2.5 mg to 10 mg daily took place over 9-12 weeks. The mean age of the patients was 64 years, 60% were male and 79% Asian. The target dosage of 10 mg daily was reached in 73% of patients with 96% of patients achieving 5 mg or 10 mg daily. During the study period uncontrolled hypertension (> 160/90) was recorded in 15% of patients, myocardial infarction or unstable angina 1.6%, heart failure 0.4%, new diabetes 0.6%. Only 9.8% of patients discontinued treatment with 5.9% attributed to treatment side-effects and 4% related to cough. The large majority of patients in a wide range of clinical practice settings with high cardiovascular risk can be treated with ramipril titrated to 10 mg daily with good tolerability.
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PMID:The HOPE TIPS: the HOPE study translated into practices. 1614 93

(1) Some angiotensin-converting-enzyme inhibitors (ACE inhibitors) reduce mortality in patients with heart failure (captopril, enalapril, ramipril and trandolapril), and in patients with recent myocardial infarction and heart failure or marked left ventricular dysfunction (captopril, ramipril and trandolapril). (2) Angiotensin II receptor antagonists, otherwise known as angiotensin receptor blockers, have haemodynamic effects similar to ACE inhibitors, but differ in their mechanism of action and certain adverse effects. (3) Five clinical trials have evaluated angiotensin II receptor antagonists (candesartan, losartan and valsartan) in terms of their effect on mortality and on the risk of clinical deterioration in patients with symptomatic heart failure, but without severe renal failure, hyperkalemia or hypotension. In these trials, candesartan and valsartan were used at much higher doses than those recommended for the treatment of arterial hypertension. (4) In patients with heart failure who were not taking an angiotensin II receptor antagonist or an ACE inhibitor at enrollment, no significant difference was found between losartan and captopril in terms of mortality or the risk of clinical deterioration. (5) In patients with heart failure who had stopped taking an ACE inhibitor because of adverse effects, candesartan had no effect on mortality as compared with placebo, but it did reduce the risk of clinical deterioration (3 fewer hospitalisations per year per 100 patients). However, candesartan was associated with adverse effects such as renal failure and hyperkalemia, especially in patients who had experienced these same adverse effects while taking an ACE inhibitor. (6) In patients with heart failure who were already taking an ACE inhibitor, adjunctive candesartan or valsartan treatment did not influence mortality in comparison to the addition of a placebo. Adding candesartan or valsartan reduced the risk of hospitalisation (between 1 and 3 fewer hospitalisations per year per 100 patients), but increased the risk of renal failure and hyperkalemia. (7) In patients with heart failure and incapacitating dyspnea despite ACE inhibitor + diuretic combination therapy, there are no trials comparing the addition of an angiotensin II receptor antagonist versus spironolactone. Adjunctive spironolactone therapy prevents 5 to 6 deaths per year per 100 patients in this setting. (8) In patients with heart failure who do not have markedly altered cardiac contractility, candesartan appears to have no clinical advantages over placebo. (9) In some of these trials, mortality was higher with angiotensin II receptor antagonist therapy than with placebo among patients who were already taking a betablocker. (10) Two trials have compared an angiotensin II receptor antagonist with an ACE inhibitor in patients with recent myocardial infarction who had heart failure or an altered left ventricular ejection fraction, but who did not have hypotension or severe renal failure. However, there are no placebo-controlled randomised trials assessing the effects of angiotensin II receptor antagonists on mortality. (11) In patients with recent myocardial infarction, these trials showed no difference in mortality between angiotensin II receptor antagonist treatment (losartan or valsartan) and captopril. They did not rule out the possibility that these angiotensin II receptor antagonists are moderately less effective than captopril. Adding valsartan to ongoing captopril therapy did not reduce mortality or morbidity as compared with placebo, but did increase the risk of adverse effects. (12) Overall, these trials confirm the advantage of angiotensin II receptor antagonists over ACE inhibitors with respect to some adverse effects (cough, skin rash, etc.). However, the two drug classes share certain serious adverse effects such as hyperkalemia, renal failure and hypotension. In one trial, angioedema was less frequent with angiotensin II receptor antagonist therapy (one less case per 500 patients).
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PMID:Angiotensin II receptor antagonists and heart failure: angiotensin-converting-enzyme inhibitors remain the first-line option. 1628 75

The Heart Outcomes Prevention Evaluation (HOPE) study demonstrated that the angiotensin-converting enzyme inhibitor, ramipril, significantly reduces mortality, myocardial infarction and stroke in high-risk cardiovascular patients, beyond the benefits from blood pressure lowering. The tolerability of ramipril 10 mg/day has been an important concern when applying these results. Following the same criteria as the HOPE study, we investigated the adverse effects profile and tolerability of 10 mg ramipril in high-risk patients at our institution. In total, 92 patients with high cardiovascular risk were eligible for this study. Initially, ramipril was prescribed 2.5 mg orally once daily, and then titrated up to 5.0, 7.5, and 10.0 mg/day at 1-month intervals. The target maintenance dose was 10 mg/day. All adverse events were recorded during at least 3 months of follow-up. After 4-6 months of the titration protocol, only 18 patients (25.3%) reached and remained on ramipril 10 mg/day; 11 (15.5%), 22 (30.9%), and 20 patients (28.2%) remained on 2.5, 5.0, and 7.5 mg/day, respectively. Twenty-one patients (22.6%) had at least one adverse event. Twelve patients (13.0%) stopped treatment because of adverse effects. A total of 23 episodes of adverse events were reported, including cough (15.1%), dizziness (6.0%), and hypotension (2.4%). Ramipril was relatively well tolerated in our study population. However, only one-quarter of our patients reached the target maintenance dose of 10 mg/day. Dry cough, dizziness, and hypotension were the major side effects. About 15% of our patients discontinued ramipril treatment, which is comparable with previous reports.
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PMID:Tolerability of ramipril 10 mg daily in high-risk cardiovascular patients in Taiwan: experience from Kaohsiung Medical University Chung-Ho Memorial Hospital. 1635 53

Drugs that inhibit the renin-angiotensin system (RAS), namely angiotensin-converting enzyme inhibitors (ACE-I) and angiotensin receptor antagonists (ARA) are gaining increasing popularity as initial medications for the management of hypertensive patients. In the year 2002, ACE-I were the most commonly prescribed drugs for the treatment of hypertension in USA. Although their antihypertensive efficacy as monotherapy is similar to other antihypertensive agents, they have the advantage of better tolerability, limited side effects and a favorable metabolic profile. When compared to other antihypertensive agents (diuretics, beta-adrenergic blockers and calcium antagonists) in large clinical trials, ACE-I and ARA provided no additional advantages regarding improvement in cardiovascular and total mortality. With the exception of the superiority of ARA in prevention of stroke, RAS inhibitors have no advantage over other agents in prevention of other cardiovascular morbid events, namely, heart failure (though ACE-I are superior to calcium antagonists), coronary heart disease and total cardiovascular events. However, there is the possibility that these agents have other benefits beyond blood pressure lowering. At equal degrees of blood pressure reduction, RAS inhibitors prevent or delay the development of diabetes mellitus and provide better end-organ protection, kidneys, blood vessels and the heart when compared with other antihypertensive agents. The combined use of ACE-I and ARA is particularly useful in organ protection. RAS inhibitors are specifically indicated in the treatment of hypertension in patients with impaired left ventricular systolic function, diabetes, proteinuria, impaired kidney function, myocardial infarction, multiple cardiovascular risk factors and possibly elderly patients. The main limitation of the ACE-I is cough and rarely angioedema. Elderly patients or those who are volume depleted or receiving large doses of diuretics or in heart failure are liable to develop hypotensive reaction and/or deterioration in kidney function.
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PMID:RAS inhibition in hypertension. 1639 19

The renin-angiotensin-aldosterone system plays a key role in the regulation of fluid and electrolyte balance. Angiotensin II receptor blockers (ARBs) inhibit angiotensin II type 1 receptors and large clinical trials have shown that they are effective in many cardiovascular diseases including hypertension, heart failure, myocardial infarction and diabetic nephropathy. They lower blood pressure effectively, are very well tolerated and can be used as monotherapy or in combination with other drug classes for the treatment of hypertension. ARBs are particularly suitable for hypertensive patients with co-morbidities such as diabetes, microalbuminuria, proteinuria, left ventricular hypertrophy and heart failure. Unlike angiotensin-converting enzyme inhibitors, ARBs do not cause persistent dry cough. For patients in whom angiotensin-converting enzyme inhibitors are indicated but not tolerated, an ARB should be considered. Periodic monitoring of renal function and electrolytes is required in patients treated with an ARB.
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PMID:Therapeutic potential of angiotensin receptor blockers in hypertension. 1673 15

Left ventricular (LV) dysfunction and/or heart failure (HF) are frequent complications of hypertension and myocardial infarction (MI), placing affected patients at increased risk of significant morbidity and premature death. Given that the renin-angiotensin-aldosterone system (RAAS) is activated and of pathophysiological importance in such patients, a strong therapeutic rationale exists to target the main effector mechanism (that is, angiotensin II [Ang II]) in order to lessen the associated morbidity and mortality burden. Angiotensin-converting enzyme (ACE) inhibitors have been shown to reduce mortality and LV dysfunction and to slow disease progression in patients with HF, including high-risk, post-MI patients. However, ACE inhibitors (ACE-Is) may not provide optimal long-term RAAS blockade (a finding that is associated with a worse prognosis) and many patients are unable to tolerate such therapy (because of troublesome dry cough, for example). In contrast, Ang II receptor blockers (ARBs) may block the RAAS more completely than ACE-Is and appear to be better tolerated. Several large-scale trials gave evaluated the efficacy of ARBs in patients with LV dysfunction and/or HF (including high-risk, post-MI patients), and have confirmed their utility as an efficacious and well-tolerated alternative to ACE-Is in this setting.
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PMID:Use of valsartan in post-myocardial infarction and heart failure patients. 1698 31

Angiotensin-converting enzyme (ACE) inhibitors improve the prognosis in mild, moderate and severe heart failure, as well as preventing the onset of heart failure in patients with chronic asymptomatic left-ventricular dysfunction and in those with reduced ejection fraction after myocardial infarction (MI). Imidapril is a long-acting ACE inhibitor that is rapidly converted in the liver to its active metabolite, imidaprilat. Maximum plasma concentrations of imidapril and imidaprilat are achieved after 2 and 5-6 hours, respectively, with corresponding elimination half-lives of 1.1-2.5 and 10-19 hours. Imidapril is used in the treatment of hypertension, chronic heart failure, acute MI and diabetic nephropathy. In patients with mild-to-moderate chronic heart failure, imidapril 10 mg once-daily increased exercise time and physical working capacity, decreased plasma atrial natriuretic peptide and brain natriuretic peptide levels and reduced blood pressure. It also improved left ventricular ejection fraction, being significantly more effective than bisoprolol, in patients with acute MI. Imidapril is well tolerated and preliminary studies suggest it has an advantage over captopril and enalapril in terms of a lower incidence of cough. In conclusion, imidapril is a well-investigated versatile ACE inhibitor for the treatment of a range of cardiovascular diseases.
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PMID:Imidapril in heart failure. 1709 51

We present 2 resected cases of thymic tuberculosis, which had been preoperatively diagnosed as invasive thymoma, using a thallium-201 ((201)Tl) single photon emission computed tomography ((201)Tl SPECT). [Patient 1] A 74-old-male with a 32-year history of steroid therapy for rheumatic arthritis was diagnosed with an anterior mediastinal tumor by routine chest CT scans after onset of myocardial infarction. [Patient 2] A 56-old-female with a 28-year history of diabetes mellitus presented with a dry cough. A chest CT demonstrated an anterior mediastinal tumor. Neither patient showed pulmonary infiltrations on chest x-ray. (201)Tl SPECT was undertaken for each patient. Abnormal findings could not be detected on a planar image of the scintigraphy; however, on SPECT images accumulations of (201)Tl were clearly detected in the anterior mediastinal mass and a thymoma was thus suspected in each case. Total thymectomy was carried out in each case and the mass then diagnosed as caseous granuloma in the thymus. Both patients are well without recurrence after operation. In patients with a (201)Tl SPECT positive anterior mediastinal tumor associated with an immunologically deficient status, and with negative findings in planar images on thallium scintigraphy, the possibility of thymic tuberculosis should be considered.
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PMID:Thymic tuberculosis preoperatively evaluated with thallium-201 SPECT: two resected cases. 1739 71

Curcumin is the active ingredient of turmeric that has been consumed as a dietary spice for ages. Turmeric is widely used in traditional Indian medicine to cure biliary disorders, anorexia, cough, diabetic wounds, hepatic disorders, rheumatism, and sinusitis. Extensive investigation over the last five decades has indicated that curcumin reduces blood cholesterol, prevents low-density lipoprotein oxidation, inhibits platelet aggregation, suppresses thrombosis and myocardial infarction, suppresses symptoms associated with type II diabetes, rheumatoid arthritis, multiple sclerosis, and Alzheimer's disease, inhibits HIV replication, enhances wound healing, protects from liver injury, increases bile secretion, protects from cataract formation, and protects from pulmonary toxicity and fibrosis. Evidence indicates that the divergent effects of curcumin are dependent on its pleiotropic molecular effects. These include the regulation of signal transduction pathways and direct modulation of several enzymatic activities. Most of these signaling cascades lead to the activation of transcription factors. Curcumin has been found to modulate the activity of several key transcription factors and, in turn, the cellular expression profiles. Curcumin has been shown to elicit vital cellular responses such as cell cycle arrest, apoptosis, and differentiation by activating a cascade of molecular events. In this chapter, we briefly review the effects of curcumin on transcription factors NF-KB, AP-1, Egr-1, STATs, PPAR-gamma, beta-catenin, nrf2, EpRE, p53, CBP, and androgen receptor (AR) and AR-related cofactors giving major emphasis to the molecular mechanisms of its action.
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PMID:Modulation of transcription factors by curcumin. 1756 8

Class I recommendations for treating patients with current or prior symptoms of heart failure with reduced left ventricular ejection fraction (LVEF) include using diuretics and salt restriction in individuals with fluid retention. Use angiotensin-converting enzyme (ACE) inhibitors, beta blockers, and angiotensin II receptor blockers if intolerant to ACE inhibitors because of cough or angioneurotic edema. Nonsteroidal anti-inflammatory drugs, most antiarrhythmic drugs, and calcium channel blockers should be avoided or withdrawn. Exercise training is recommended. Implant cardioverter-defibrillator (ICD) is recommended in individuals with a history of cardiac arrest, ventricular fibrillation, or hemodynamically unstable ventricular tachycardia. ICD is indicated in patients with ischemic heart disease for at least 40 d post-myocardial infarction or nonischemic cardiomyopathy, an LVEF of 30% or less, New York Heart Association (NYHA) class II or III symptoms on optimal medical therapy, and an expectation of survival of at least 1 yr. Cardiac resynchronization therapy should be used in individuals with an LVEF of 35% or below, NYHA class III or IV symptoms despite optimal therapy, and a QRS duration greater than 120 ms. An aldosterone antagonist can be added in selected patients with moderately severe to severe symptoms of heart failure who can be carefully monitored for renal function and potassium concentration (serum creatinine should be <or=2.5 mg/dL in men and <or=2.0 mg/dL in women; serum potassium should be <5.0 mEq/L).
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PMID:Treatment of heart failure with decreased left ventricular ejection fraction. 1789 26


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