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In this large clinical trial, aspirin plus extended-release dipyridamole was found to have an efficacy similar to that of clopidogrel in the prevention of recurrent stroke. However, aspirin plus extended-release dipyridamole resulted in more bleeding, including intracranial bleeding. The results will help guide therapy for secondary stroke prevention. Aspirin plus extended-release dipyridamole was found to have an efficacy similar to that of clopidogrel in the prevention of recurrent stroke. However, aspirin plus extended-release dipyridamole resulted in more bleeding, including intracranial bleeding. Recurrent stroke is an important vascular event affecting the life of survivors of ischemic stroke. 1 Multiple randomized trials have proved the efficacy of antiplatelet agents for the prevention of recurrent stroke after noncardioembolic stroke. 2 – 11 Antiplatelet options for the prevention of recurrent stroke include aspirin (50 mg to 325 mg per day), the combination of low-dose aspirin and extended-release dipyridamole, and clopidogrel alone. 12 , 13 Aspirin has been shown to reduce the risk of stroke recurrence by about 23% as compared with placebo. 7 Studies of clopidogrel have suggested an 8% relative risk reduction of stroke recurrence, as compared with aspirin, among . . .

In this randomized trial, the discontinuation of renin–angiotensin system inhibitors in patients with advanced chronic kidney disease did not lead to a significant between-group difference in the long-term rate of decline in the eGFR.

Among patients with recent MI, therapy with a polypill containing aspirin, ramipril, and atorvastatin led to a lower incidence of major adverse cardiovascular events at a median of 3 years than usual care.

In a multicenter trial, 20,332 patients who had recently had an ischemic stroke were randomly assigned to receive either telmisartan or placebo. All patients also received medications for blood-pressure control at the investigators' discretion. At a mean follow-up of 2.5 years, there was no significant difference between the two study groups in the rates of recurrent stroke or major cardiovascular events. Patients who had recently had an ischemic stroke were randomly assigned to receive either telmisartan or placebo. At a mean follow-up of 2.5 years, there was no significant difference between the study groups in the rates of recurrent stroke or major cardiovascular events. Stroke is the second most frequent cause of death in the world and is responsible for about 5 million deaths each year. 1 An additional 15 million persons have nonfatal strokes, with about a third having disabling consequences. Elevated blood pressure is the strongest risk factor for stroke, and lowering of blood pressure, especially in patients with substantially elevated levels (e.g., systolic pressure, >160 mm Hg), reduces the risk of stroke. 2 After a stroke, lowering blood pressure with a combination of an angiotensin-converting–enzyme (ACE) inhibitor and a diuretic reduced rates of recurrent stroke in the Perindopril Protection against Recurrent Stroke Study . . .

In a randomized trial, 5661 patients with acute myocardial infarction and a reduced left ventricular ejection fraction, pulmonary congestion, or both were assigned to receive either sacubitril–valsartan or ramipril. At a median of 22 months, there was no significant difference between the two groups in the incidence of death from cardiovascular causes or incident heart failure.

Purpose Non-steroidal anti-inflammatory drugs (NSAIDs) are known to antagonize the effects of antihypertensive drugs, and these associations can lead to an increase in arterial blood pressure. However, the impact of NSAIDs on hypertension treatment management in large-scale populations remains poorly evaluated. We examined whether the introduction of NSAID into the treatment regimen would induce an intensification of hypertension treatment (defined as the introduction of a new antihypertensive drug). Methods We conducted a cohort study involving 5,710 hypertensive subjects included in the French health insurance system database who had been treated and stabilized with their antihypertensive therapy and not exposed to any NSAID between 1 April 2005 and 1 April 2006. The maximum follow-up duration was 4 years. Results Adjusted hazard ratios (HR) for hypertension treatment intensification were 1.34 [95 % confidence interval (CI) 1.05–1.71] for NSAIDs in general, 1.79 (95 % CI 1.15–2.78) for diclofenac and 2.02 (95 % CI:1.09–3.77) for piroxicam. There were significant interactions between NSAIDs and angiotensin converting enzyme inhibitors (ACEIs; HR  4.09, 95 % CI 2.02–8.27) or angiotensin receptor blockers (ARBs; HR 3.62, 95 % CI 1.80–7.31), but not with other antihypertensive drugs. Conclusions Exposure to NSAIDs leads to an intensification of hypertension treatment, especially in patients treated with ACEIs or ARBs. Renin–angiotensin system blockers should be avoided whenever NSAIDs are prescribed.

The angiotensin receptor–neprilysin inhibitor LCZ696 was compared with the ACE inhibitor enalapril in patients with advanced heart failure. LCZ696 was superior to enalapril in all outcomes. Neprilysin inhibition may replace ACE inhibition for the treatment of heart failure. Angiotensin-converting–enzyme (ACE) inhibitors have been the cornerstone of the treatment for heart failure and a reduced ejection fraction for nearly 25 years, since enalapril was shown to reduce the risk of death in two trials. 1 , 2 Long-term treatment with enalapril decreased the relative risk of death by 16% among patients with mild-to-moderate symptoms. 2 The effect of angiotensin-receptor blockers (ARBs) on mortality has been inconsistent, 3 , 4 and thus, these drugs are recommended primarily for patients who have unacceptable side effects (primarily cough) while receiving ACE inhibitors. Subsequent studies showed that the use of beta-blockers and mineralocorticoid-receptor antagonists, when added to ACE . . .

Patients with acute decompensated heart failure were randomly assigned to receive sacubitril–valsartan or enalapril. At 8 weeks, the sacubitril–valsartan group had a greater reduction in the N-terminal pro–B-type natriuretic peptide concentration than the enalapril group.

Three drug classes (mineralocorticoid receptor antagonists [MRAs], angiotensin receptor–neprilysin inhibitors [ARNIs], and sodium/glucose cotransporter 2 [SGLT2] inhibitors) reduce mortality in patients with heart failure with reduced ejection fraction (HFrEF) beyond conventional therapy consisting of angiotensin-converting enzyme (ACE) inhibitors or angiotensin receptor blockers (ARBs) and β blockers. Each class was previously studied with different background therapies and the expected treatment benefits with their combined use are not known. Here, we used data from three previously reported randomised controlled trials to estimate lifetime gains in event-free survival and overall survival with comprehensive therapy versus conventional therapy in patients with chronic HFrEF. In this cross-trial analysis, we estimated treatment effects of comprehensive disease-modifying pharmacological therapy (ARNI, β blocker, MRA, and SGLT2 inhibitor) versus conventional therapy (ACE inhibitor or ARB and β blocker) in patients with chronic HFrEF by making indirect comparisons of three pivotal trials, EMPHASIS-HF (n=2737), PARADIGM-HF (n=8399), and DAPA-HF (n=4744). Our primary endpoint was a composite of cardiovascular death or first hospital admission for heart failure; we also assessed these endpoints individually and assessed all-cause mortality. Assuming these relative treatment effects are consistent over time, we then projected incremental long-term gains in event-free survival and overall survival with comprehensive disease-modifying therapy in the control group of the EMPHASIS-HF trial (ACE inhibitor or ARB and β blocker). The hazard ratio (HR) for the imputed aggregate treatment effects of comprehensive disease-modifying therapy versus conventional therapy on the primary endpoint of cardiovascular death or hospital admission for heart failure was 0·38 (95% CI 0·30–0·47). HRs were also favourable for cardiovascular death alone (HR 0·50 [95% CI 0·37–0·67]), hospital admission for heart failure alone (0·32 [0·24–0·43]), and all-cause mortality (0·53 [0·40–0·70]). Treatment with comprehensive disease-modifying pharmacological therapy was estimated to afford 2·7 additional years (for an 80-year-old) to 8·3 additional years (for a 55-year-old) free from cardiovascular death or first hospital admission for heart failure and 1·4 additional years (for an 80-year-old) to 6·3 additional years (for a 55-year-old) of survival compared with conventional therapy. Among patients with HFrEF, the anticipated aggregate treatment effects of early comprehensive disease-modifying pharmacological therapy are substantial and support the combination use of an ARNI, β blocker, MRA, and SGLT2 inhibitor as a new therapeutic standard. None.

In a multicenter placebo-controlled study, patiromer, a nonabsorbable potassium binder, led to a reduction in serum potassium levels in patients with chronic kidney disease and hyperkalemia who were receiving renin–angiotensin–aldosterone system (RAAS) inhibitors. Hyperkalemia is associated with life-threatening cardiac arrhythmias and increased mortality. 1 Patients at the highest risk for hyperkalemia are those with stage 3 or higher chronic kidney disease, with or without diabetes or heart failure, who are being treated with drugs that inhibit renal potassium excretion, particularly inhibitors of the renin–angiotensin–aldosterone system (RAAS). 1 – 4 Outpatient treatment of hyperkalemia is limited by the lack of effective agents. 4 Sodium polystyrene sulfonate and calcium polystyrene sulfonate may cause serious gastrointestinal adverse events 5 – 8 as well as less serious gastrointestinal side effects that may be difficult for patients to tolerate, which together typically limit their . . .