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In patients with myocardial infarction and anemia, a liberal transfusion strategy led to fewer deaths and heart attacks than a restricted transfusion strategy, but the difference was of borderline significance.

Patients who develop heart failure (HF) after an acute myocardial infarction (AMI) are at higher risk of adverse fatal and nonfatal outcomes. Published studies on the incidence and associations of HF after infarction have been contradictory, with some reporting increasing and others decreasing incidence. Between 2000 and 2015, 109,717 patients admitted for a first AMI in New Jersey were discharged alive. In the 15 years from 2000 to 2015, the rates of admission for HF in AMI patients who were discharged alive decreased by 60%, from 3.48% to 1.4%, at 1-year follow-up. At 5 years of follow-up, the decline was more pronounced, from 7.21% to 1.4%, an 80% decline. All-cause death, and the combined end point of admission for HF or death, showed decreasing trends. Cox regression indicated a decrease in the risk of admission for HF over time (hazard ratio [HR] 0.955, 95% confidence interval [CI] 0.949 to 0.961). Younger age, male gender, and commercial insurance were associated with lower HRs for HF (p <0.001), whereas history of hypertension, diabetes, kidney, or lung disease were associated with higher HRs (p <0.001). There was no significant difference in the rate of HF between subendocardial and transmural AMI (adjusted OR was 0.96, CI 0.90 to 1.03, p = 0.241). Revascularization was associated with a marked decrease in HF admissions (adjusted OR 0.22, 95% CI 0.19 to 0.25, p <0.001 for percutaneous coronary intervention and OR 0.44, 95% CI 0.38 to 0.51, p <0.001 for CABG). In conclusion, the rate of admission for HF after discharge for a first myocardial infarction as well as all-cause death decreased markedly from 2000 to 2015.

We examined the association of orthostatic hypertension with all-cause mortality in the active treatment and placebo randomized groups of the Systolic Hypertension in the Elderly Program (SHEP). SHEP was a multicenter, randomized, double-blind, placebo-controlled clinical trial of the effect of chlorthalidone-based antihypertensive treatment on the rate of occurrence of stroke among older persons with isolated systolic hypertension (ISH). Men and women aged 60 years and above with ISH defined by a systolic blood pressure (SBP) of 160 mm Hg or higher and diastolic blood pressure lower than 90 mm Hg were randomized to chlorthalidone-based stepped care therapy or matching placebo. Among 4736 SHEP participants, 4073 had a normal orthostatic response, 203 had orthostatic hypertension, and 438 had orthostatic hypotension. Compared with normal response, orthostatic hypertension was associated with higher all-cause mortality at 4.5 and 17 years in analyses adjusted for age, gender, treatment, SBP, and pulse pressure (PP, HR 1.87, 95% CI 1.30–2.69, p = 0.0007; HR 1.40, 95% CI 1.17–1.68, p = 0.0003, respectively). These associations remained significant after additional adjustment for risk factors and comorbidities (HR 1.43, 95% CI 0.99–0.08, p = 0.0566 at 4.5 years, and HR 1.27, 95% CI 1.06–1.53, p = 0.0096 at 17 years). The increased risk of all-cause mortality associated with orthostatic hypertension was observed in both the active and placebo groups without significant interaction between randomization group and the effect on mortality. Orthostatic hypertension is associated with future mortality risk, is easily detected, and can be used in refining cardiovascular risk assessment.

This post hoc analysis of the Systolic Blood Pressure Intervention Trial (SPRINT) examined the performance of chlorthalidone (C) versus amlodipine (A) monotherapies. ANOVA was used to analyze the differences in systolic blood pressure (SBP) response between C and A. Logistic regression was used to examine monotherapy failure (adding a second antihypertensive agent or switching to a different antihypertensive agent) rates. Four hundred ninety‐one participants were treated with C monotherapy (n = 210, mean dose = 22 mg/day) or A monotherapy (n = 281, mean dose = 7 mg/day). There was a significant difference in mean SBP reduction between the C and A monotherapies at the third visit (higher reduction with A, adjusted p = .018). Unadjusted analysis showed a higher failure with C in the standard treatment group. Although the average SBP at failure was higher and above the 140 mm Hg cutoff that indicated monotherapy failure with A (142.60) compared with C (138.40), more participants on C failed despite having SBP below the 140 cutoff. This was probably due to decisions made by the investigative teams to change the antihypertensive regimen, because, in their opinion, the clinical picture required it. After adjusting for baseline characteristics, C had higher failure than A only in the standard treatment group (1.64 odds ratio [OR], 95% CI 1.06–2.56, p = .028). A sub‐analysis including participants who had never used antihypertensive treatment before randomization had similar results (2.57 OR, 95% CI 1.34–5.02, p = .004). Overall, in SPRINT chlorthalidone was associated with higher monotherapy failure than amlodipine in the standard treatment group because of decisions of the investigative teams.

Human myocardium has a complex and anisotropic 3D fiber pattern. It remains unknown, however, when in fetal life this anisotropic pattern develops and whether the human heart is structurally fully mature at birth. We aimed here to use diffusion tensor MRI (DTI) tractography to characterize the evolution of fiber architecture in the developing human fetal heart. Human fetal hearts (n = 5) between 10-19 weeks of gestation were studied. The heart from a 6-day old neonate and an adult human heart served as controls. The degree of myocardial anisotropy was measured by calculating the fractional anisotropy (FA) index. In addition, fiber tracts were created by numerically integrating the primary eigenvector field in the heart into coherent streamlines. At 10-14 weeks the fetal hearts were highly isotropic and few tracts could be resolved. Between 14-19 weeks the anisotropy seen in the adult heart began to develop. Coherent fiber tracts were well resolved by 19 weeks. The 19-week myocardium, however, remained weakly anisotropic with a low FA and no discernable sheet structure. The human fetal heart remains highly isotropic until 14-19 weeks, at which time cardiomyocytes self-align into coherent tracts. This process lags 2-3 months behind the onset of cardiac contraction, which may be a prerequisite for cardiomyocyte maturation and alignment. No evidence of a connective tissue scaffold guiding this process could be identified by DTI. Maturation of the heart's sheet structure occurs late in gestation and evolves further after birth.

Purpose of ReviewThis study aims to examine current knowledge on the occurrence, pathophysiology, and treatment of angioedema among patients who receive angiotensin-converting enzyme inhibitors.Recent FindingsAngiotensin-converting enzyme inhibitors (ACE-I), a medication class used by an estimated 40 million people worldwide, are associated with angioedema that occurs with incidence ranging from 0.1 to 0.7%. The widespread use of ACE-I resulted in one third of all emergency department visits for angioedema. Angioedema occurs more frequently in African Americans, smokers, women, older individuals, and those with a history of drug rash, seasonal allergies, and use of immunosuppressive therapy. The pathophysiology of ACE-I-induced angioedema involves inhibition of bradykinin and substance P degradation by ACE (kininase II) leading to vasodilator and plasma extravasation. Treatment modalities include antihistamines, steroids, and epinephrine, as well as endotracheal intubation in cases of airway compromise. Patients with a history of ACE-I-induced angioedema should not be re-challenged with this class of agents, as there is a relatively high risk of recurrence.ConclusionACE-I are frequently used therapeutic agents that are associated with angioedema. Their use should be avoided in high-risk individuals and early diagnosis, tracheal intubation in cases of airway compromise, and absolute avoidance of re-challenge are important.

We compared stroke rates associated with coronary artery bypass grafting (CABG), both on-pump and off-pump, and percutaneous coronary intervention (PCI) with both drug-eluting stent (DES) and bare-metal stent (BMS) and the impact on 30-day and 1-year all-cause mortality. The Myocardial Infarction Data Acquisition System database was used to study patients who had on-pump CABG (n = 47,254), off-pump CABG (n = 19,118), and PCI with BMS (n = 46,641), and DES (n = 115,942) in New Jersey from 2002 to 2012. Multiple logistic and Cox proportional hazard models were used to compare the risk of stroke and mortality. Adjustments were made for demographics, year of hospitalization, and co-morbidities. The rate of postprocedural stroke was lowest with DES (0.5%), followed by BMS (0.6%), off-pump CABG (1.3%), and on-pump CABG (1.8%). After adjustment, on-pump CABG had a higher risk of stroke compared with off-pump (odds ratio 1.36, 95% CI 1.18 to 1.56, p <0.0001). DES had lower risk of stroke compared with off-pump CABG (odds ratio 0.64, 95% CI 0.55 to 0.74, p <0.0001). There was a significant excess risk of 1-year mortality due to the interaction between stroke and procedure type (on-pump vs off-pump CABG and PCI with DES vs BMS; p value for interaction = 0.02). In conclusion, in this retrospective analysis of nonrandomized data from a statewide database, PCI with DES was associated with the lowest rate of postprocedural stroke, and off-pump CABG had a lower rate of postprocedural stroke than on-pump CABG; there was an excess 1-year mortality risk with on-pump versus off-pump CABG and with DES versus BMS in patients with stroke.

We examined the effect of chlorthalidone-based stepped care on the competing risks of cardiovascular (CV) versus non-CV death in the Systolic Hypertension in the Elderly Program (SHEP). Participants were randomly assigned to chlorthalidone-based stepped-care therapy (n = 2,365) or placebo (n = 2,371) for 4.5 years, and all participants were advised to take active therapy thereafter. At the 22-year follow-up, the gain in life expectancy free from CV death in the active treatment group was 145 days (95% confidence interval [CI] 23 to 260, p = 0.012). The gain in overall life expectancy was smaller (105 days, 95% CI −39 to 242, p = 0.073) because of a 40-day (95% CI −87 to 161) decrease in survival from non-CV death. Compared with an age- and gender-matched cohort, participants had markedly higher overall life expectancy (Wilcoxon p = 0.00001) and greater chance of reaching the ages of 80 (81.3% vs 57.6%), 85 (58.1% vs 37.4%), 90 (30.5% vs 22.0%), 95 (11.9% vs 8.8%), and 100 years (3.7% vs 2.8%). In conclusion, Systolic Hypertension in the Elderly Program participants had higher overall life expectancy than actuarial controls and those randomized to active therapy had longer life expectancy free from CV death but had a small increase in the competing risk of non-CV death.

The benefits of reducing blood pressure on the risks of major cardiovascular disease are well established, but uncertainty remains about the comparative effects of different blood-pressure-lowering regimens. We aimed to estimate effects of strategies based on different drug classes (angiotensin-converting-enzyme [ACE] inhibitors, calcium antagonists, angiotensin-receptor blockers [ARBs], and diuretics or β blockers) or those targeting different blood pressure goals, on the risks of major cardiovascular events and death. We did seven sets of prospectively-designed overviews with data from 29 randomised trials (n=162 341). The trial eligibility criteria, primary outcomes, and main hypotheses were specified before the result of any contributing trial was known. In placebo-controlled trials the relative risks of total major cardiovascular events were reduced by regimens based on ACE inhibitors (22%; 95% CI 17–27) or calcium antagonists (18%; 5–29). Greater risk reductions were produced by regimens that targeted lower blood pressure goals (15%; 5–24). ARB-based regimens reduced the risks of total major cardiovascular events (10%; 4–17) compared with control regimens. There were no significant differences in total major cardiovascular events between regimens based on ACE inhibitors, calcium antagonists, or diuretics or β blockers, although ACE-inhibitor-based regimens reduced blood pressure less. There was evidence of some differences between active regimens in their effects on cause-specific outcomes. For every outcome other than heart failure, the difference between randomised groups in achieved blood pressure reduction was directly related to the observed difference in risk. Treatment with any commonly-used regimen reduces the risk of total major cardiovascular events, and larger reductions in blood pressure produce larger reductions in risk.

Clinical guidelines from the United States and Europe do not recommend treatment with statins for primary prevention in patients with hypercholesterolemia who are older than 75 years. Data from 35 randomized controlled trials in this age group where statin therapy for primary prevention was compared with placebo or usual care were analyzed. Using all-cause death as the outcome, we performed 2 types of analyses: frequentist and Bayesian. Frequentist analysis indicated no significant difference in mortality between cases (on statins) and controls (on placebo or usual care, p = 0.16). However, in the Bayesian analysis, patients >75 years had lower mortality from treatment with statins (p = 0.03). In conclusion, Bayesian analysis indicates a definite, statistically significant and clinically relevant benefit of statin treatment for primary prevention in patients >75 years of age.