Background: Navy beans and rice bran demonstrate efficacy to regulate serum cholesterol in hypercholesterolemic adults; however, the cardiovascular disease (CVD) protective properties of these foods in children are unknown and merit investigation. Objective: The objectives were to determine whether cooked navy bean powder (NBP) and/or heat-stabilized rice bran (RB) supplementation is tolerable, improves dietary fiber intake in children, and modulates lipid profiles. Methods: Children aged 8 to 13 years at risk for CVD due to abnormal lipids were recruited. Elevated cholesterol levels were defined as total cholesterol ≥180 mg/dL and high-density lipoprotein (HDL) <60 mg/dL; low-density lipoprotein (LDL) ≥100 mg/dL and HDL <60 mg/dL; or non-HDL >100 mg/dL and HDL <60 mg/dL. Participants completed a pilot 4-week, randomized controlled, 4-arm dietary intervention. They consumed study-provided muffins or a smoothie daily that included 0 g NBP or RB (control), 17.5 g NBP, 15 g RB, or a combination 9 g NBP + 8 g RB. Fasting blood was collected at baseline and week 4. Participants also completed 3-day food logs and gastrointestinal health questionnaires. Results: Thirty-eight children completed the trial (n = 9 control, n = 10 NBP, n = 9 RB, and n = 10 NBP + RB groups). Only 3 participants withdrew due to noncompliance of required food consumption. Participants in the intervention groups significantly increased intake of NBP and RB at week 4 (p≤.01). The NBP and NBP + RB groups increased total fiber intake from baseline to week 4 (p=.02 and p=<.01, respectively). HDL-cholesterol was higher in NBP-group participants compared to control at week 4 (P = .02). Conclusion: Increasing NBP and/or RB intake is tolerable for children, and our findings suggest higher daily intakes are needed for a longer duration to induce favorable changes across multiple serum lipid parameters.
Background: Myocardial infarction with nonobstructive coronary arteries (MINOCA) is an underrecognized clinical problem in patients presenting with acute coronary syndrome. Various clinical disorders lead to MINOCA thus making treatment and diagnosis a challenge. We aimed to compare the clinical factors and outcomes of patients with MINOCA versus obstructive disease [myocardial infarction due to coronary artery disease (MI-CAD)] in a largely rural health system. Methods: Between May 1, 2009 and June 24, 2019, all consecutive ST-segment elevation myocardial infarction patients at Essentia Health were prospectively examined. We categorized patients into MI-CAD (obstructive plaque ≥ 50% with revascularization) or MINOCA (obstructive plaque < 50% with exclusion of other alternative cause). Outcomes included 30-day and 1-year all-cause mortality, 30-day all-cause readmission and 30-day cardiac readmission. Results: There were 2170 patients included in the study; 2097 (96.6 %) had MI-CAD and 73 (3.4%) met the definition of MINOCA. Within the MINOCA group, the 3 most common presentations were supply-demand mismatch (28.8%), spontaneous coronary artery dissection (9.6%), and other etiology (60.3%). Only 10 (13 %) MINOCA patients had cardiac magnetic resonance imaging studies obtained within 6 months. MINOCA patients were younger 61.6 versus 63.4 years with higher left ventricular function 51.6% versus 50.4% with less likelihood of prior myocardial infarction 4.1% versus 15.5% or congestive heart failure 2.7% versus 6.3% (P < 0.05). Compared with MI-CAD patients, MINOCA patients had similar 30-day mortality (7.1% vs. 8.2%; P = 0.70), 1-year mortality (10.4% vs. 8.2 %; P = 0.55), and 30-day cardiac readmission (8.7% vs. 9.6%; P = 0.29). MINOCA patients were less likely to be discharged on aspirin, betablockers, angiotensin-converting enzyme inhibitor/angiotensin receptor blockers, or statins (P < 0.05). Conclusion:Though there was no difference in readmission and mortality between MINOCA and MI-CAD; use of secondary prevention medications and cardiac rehabilitation referral was low in MINOCA patients. Prospective studies will be relevant to assess effective medical therapy to improve outcomes in MINOCA patients.
Background Digoxin acutely increases cardiac output in patients with pulmonary arterial hypertension (PAH) and right ventricular failure; however, the effects of chronic digoxin use in PAH are unclear. Methods and Results Data from the Minnesota Pulmonary Hypertension Repository were used. The primary analysis used likelihood of digoxin prescription. The primary end point was a composite of all‐cause mortality or heart failure (HF) hospitalization. Secondary end points included all‐cause mortality, HF hospitalization, and transplant‐free survival. Multivariable Cox proportional hazards analyses determined the hazard ratios (HR) and 95% CIs for the primary and secondary end points. Among 205 patients with PAH in the repository, 32.7% (n=67) were on digoxin. Digoxin was more often prescribed to patients with severe PAH and right ventricular failure. After propensity score‐matching, 49 patients were digoxin users, and 70 patients were nonusers; of these 31 (63.3%) in the digoxin group and 41 (58.6%) in nondigoxin group met the primary end point during a median follow‐up time of 2.1 (0.6–5.0) years. Digoxin users had a higher combined all‐cause mortality or HF hospitalization (HR, 1.82 [95% CI, 1.11–2.99]), all‐cause mortality (HR, 1.92 [95% CI, 1.06–3.49]), HF hospitalization (HR, 1.89 [95% CI, 1.07–3.35]), and worse transplant‐free survival (HR, 2.00 [95% CI, 1.12–3.58]) even after adjusting for patient characteristics and severity of PAH and right ventricular failure. Conclusions In this retrospective, nonrandomized cohort, digoxin treatment was associated with greater all‐cause mortality and HF hospitalization, even after multivariate correction. Future randomized controlled trials should assess the safety and efficacy of chronic digoxin use in PAH.
Current ST-segment elevation myocardial infarction (STEMI) guidelines require persistent electrocardiogram ST-segment elevation, cardiac enzyme changes, and symptoms of myocardial ischemia. Chest pain is the determinant symptom, often measured using an 11-point scale (0-10). Greater severity of chest pain is presumed to be associated with a stronger likelihood of a true positive STEMI diagnosis. This retrospective observational cohort study considered consecutive STEMI patients from May 02, 2009 to December 31, 2018. Analysis of standard STEMI metrics included positive electrocardiogram-to-device and first medical contact-todevice times, presence of comorbidities, false-positive diagnosis, 30-day and 1-year mortality, and 30-day readmission. Chest pain severity was assessed upon admission to the primary percutaneous coronary intervention hospital. We analyzed 1409 STEMI activations (69% male, 66.3 years old ± 13.7 years). Of these, 251 (17.8%) had no obstructive lesion, consistent with false-positive STEMI. Four hundred sixty-six (33.1%) reported chest pain rating of 0 on admission, 378 (26.8%) reported mild pain (1-3), 300 (21.3%) moderate (4-6), and 265 (18.8%) severe (7-10). Patients presenting without chest pain had a significantly higher rate of false-positive STEMI diagnosis. Increasing chest pain severity was associated with decreased time from first medical contact to device, and decreased in-hospital, 30-day and 1-year mortality. Severity of chest pain on admission did not correlate to the likelihood of a truepositive STEMI diagnosis, although it was associated with improved patient prognosis, in the form of improved outcomes, and shorter times to reperfusion.
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