After review of the literature, I conclude that clinical trials may be unethical.
After review of the literature, I conclude that clinical trials may be unethical.
Approximately 80% of patients with hypertension in the Internal Medicine Clinic were uncontrolled (BP > 130/80 mmHg), according to the 2017 American College of Cardiology (ACC)/American Heart Association (AHA) hypertension guidelines, leading to increased morbidity and mortality. The aim of this quality improvement (QI) was to improve BP control <130/80 from the baseline rates of 20%–30% and <140/90 from the baseline rates of 40%–60% between ages of 18–75 years, within 12 months.
We used the Plan-Do-Study-Act method. A multidisciplinary QI team identified barriers by fish bone diagram. Barriers included: 1) Physicians' knowledge gap and clinical inertia in optimization of medications, and 2) Patients' nonadherence to medication and appointments. The outcome measures were the percentage of patients with BP < 140/90 and < 130/80. Process measures included: 1) attendance rates of physician and nurses at educational sessions, 2) medication reconciliation completion rates and 3) care guide order rates. Key interventions were: 1) physicians and nurses' education regarding ACC/AHA guidelines, 2) patient education and engagement and 3) enhancement of health information technology. Data analysis was performed using monthly statistical process control charts.
We achieved 62.6% (n = 885/1426) for BP < 140/90 and 24.47% (n = 349/1426) for BP < 130/80 within 12 months project period. We sustained and exceeded at 72.64% (n = 945/1301) for BP < 140/90 and 44.58% (n = 580/1301) for BP < 130/80 during the 10 months post-project period.
Overcoming physician clinical inertia, enhancing patient adherence to appointments and medications, and a high functioning multidisciplinary team were the key drivers for the success.
Patients with systemic lupus erythematosus (SLE) are at higher risk for coronary artery disease (CAD) particularly at a younger age. We sought to determine the effect of risk factors on the prevalence of CAD in age stratified hospitalized patients with SLE.
The National Inpatient Sample (NIS) was queried for hospitalized patients with SLE during the years 2010–2015, and a control group without SLE. The study sample was stratified by age, 18–35 years, 36–55 years, and adults >55 years. The effect of SLE and traditional Framingham risk factors on the prevalence of CAD were assessed. Dominance analysis allowed for ranking of CAD risk factors in each age group.
A total 167,466 patients were matched to an equal number of controls. 88.8% were women, 48.5% Caucasian and 29% African-American. In lupus patients 18–35 years prevalent risk factors included hyperlipidemia, hypertension, hypercoagulability and CKD. Diabetes and depression ranked least important. In middle and older patients, traditional risk factors were dominant. In adults >55 years the prevalence of CAD appears higher in Caucasians whereas in young patients 18–35 years, African Americans are dominant.
CAD in the young adult patient with SLE is represented predominately by an African-American population and it is dominated by a hypercoagulable state and a less significant role for diabetes. In the lupus cohort over 55 years, which is predominantly Caucasian, SLE specific factors are less significant.
The estimated pulse-wave velocity (ePWV) as measure for arterial wall stiffness is associated with an increased risk of cardiovascular disease (CVDs) and all-cause death in Western populations. We investigated the association between ePWV and the incidence of CVDs (myocardial infarction, cerebral infarction, cerebral hemorrhage) and all-cause death in Chinese. The community-based longitudinal Kailuan Study included 98,348 participants undergoing biennial clinical examinations. During a mean follow-up of 10.32 ± 2.14 years, 6967 CVD events (myocardial infarction, n = 1610; cerebral infarction, n = 4634; cerebral hemorrhage, n = 1071) and 9780 all-cause deaths occurred. Stratified by age, sex and presence of cardiovascular risk factors, the incidence of CVDs and all-cause death were higher (P < 0.01) in individuals with ePWV values ≥ 10 m/s than in those with ePWV values < 10 m/s. After adjusting for age, age squared and other conventional cardiovascular risk factors, an ePWV value of ≥10 m/s or each ePWV increase by 1 m/s increased (P < 0.01) the risk for CVDs by 32% (Hazard ratio (HR):1.32; 95% confidence interval (CI):1.23–1.42) and 22% (HR:1.22; 95%CI:1.18–1.27), respectively, and increased the risk for all-cause death significantly (P < 0.01) by 28% (HR:1.28; 95%CI:1.20–1.37) and 10% (HR:1.10; 95%CI:1.07–1.13), respectively. The mean brachial-ankle PWV, measured in 43,208 individuals, was 15.30 ± 3.51 cm/s, with a mean difference of 6.45 m/s (95% limits of agreement:1.24–11.7) to the ePWV. Independently of cardiovascular risk factors, ePWV was associated with CVDs and all-cause mortality in Chinese.
Diabetic kidney disease (diabetic nephropathy), one of the most serious renovascular diabetic complication represents the leading cause of chronic kidney disease worldwide and is characterized clinically by impaired renal functional indices, hypertension, systemic and renal hemodynamic changes and pathologically by a spectrum of glomerulotubulointerstitial and vascular lesions. Diabetic nephropathy is initiated by persistent hyperglycemia and glomerular hyperfiltration and, if untreated, progresses to increasing albuminuria, declining glomerular filtration rate (GFR), development of end-stage renal failure (ESRF) and or enhanced risk of poor cardiovascular outcomes. The emergence of sodium glucose co-transporter 2 (SGLT2) inhibitors, a novel class of antidiabetic drugs endowed with a wide range of pleiotropic actions revolutionized care of diabetes and its complications. These drugs reduce major cardiovascular events, heart failure hospitalization, rate of progression of albuminuria, and decline in GFR in both diabetic and non-diabetic patients with preserved or impaired renal function and development of ESRF.
Short sleep duration is a contributor to cardiovascular disease (CVD) events and mortality. Short sleep duration is associated with an increased risk of high clinic blood pressure (BP). BP measured outside the clinic using 24-h ambulatory blood pressure monitoring (ABPM) is a better predictor of an individual's CVD risk. We examined the association between objectively-assessed sleep duration and 24-h ambulatory blood pressure (ABP).
A total of 893 working adults underwent sleep and ABPM. Participants were fitted with an ABPM device, and measures were taken at 28–30 min intervals. Objective sleep duration, and times of wakefulness and sleep during the 24-h ABPM period were derived from wrist-worn actigraphy. Linear regression, adjusted for age, sex, race/ethnicity, body mass index, smoking status, and diabetes were conducted on the relationship between sleep duration and the ABP measures.
Mean age of participants (final n = 729, 59.5% female, 11.9% Hispanic) was 45.2 ± 10.4 y. Mean actigraphy-derived sleep duration was 6.8 ± 1.2 h. Sleep duration <6 h was associated with a 1.73 mmHg higher 24-h systolic BP (p = 0.031) and 2.17 mmHg higher 24-h diastolic BP (p < 0.001). Shorter sleep duration was not associated with mean awake or asleep systolic BP (p = 0.89 and p = 0.92) or mean awake or asleep diastolic BP (p = 0.30 and p = 0.74).
To our knowledge, this is the largest study conducted which assessed sleep duration objectively while measuring 24-h ABP. Shorter sleep duration is associated with higher 24-h BP and potentially cardiovascular risk.
The impact of the 2017 American College of Cardiology (ACC)/American Heart Association (AHA) guidelines for diagnosis and management of hypertension on the prevalence of hypertension in India is unknown.
We analyzed data from the Cardiac Prevent 2015 survey to estimate the change in the prevalence of hypertension. The JNC8 guidelines defined hypertension as a systolic blood pressure of ≥140 mmHg or diastolic blood pressure of ≥90 mmHg. The 2017 ACC/AHA guidelines define hypertension as a systolic blood pressure of ≥130 mmHg or diastolic blood pressure of ≥80 mmHg. We standardized the prevalence as per the 2011 census population of India. We also calculated the prevalence as per the World Health Organization (WHO) World Standard Population (2000–2025).
Among 180,335 participants (33.2% women), the mean age was 40.6 ± 14.9 years (41.1 ± 15.0 and 39.7 ± 14.7 years in men and women, respectively). Among them, 8,898 (4.9%), 99,791 (55.3%), 35,694 (11.9%), 23,084 (12.8%), 9,989 (5.5%) and 2,878 (1.6%) participants belonged to age group 18–19, 20–44, 45–54, 55–64, 65–74 and ≥ 75 years respectively. The prevalence of hypertension according to the JNC8 and 2017 ACC/AHA guidelines was 29.7% and 63.8%, respectively- an increase of 115%. With the 2011 census population of India, this suggests that currently, 486 million Indian adults have hypertension according to the 2017 ACC/AHA guidelines, an addition of 260 million as compared to the JNC8 guidelines.
According to the 2017 ACC/AHA guidelines, 3 in every 5 Indian adults have hypertension.
The role of inflammation in the development of hypertension remains incompletely understood. While single inflammatory mediators have been shown to associate with changes in blood pressure (ΔBP), the role of clusters of inflammatory mediators has been less comprehensively explored. We therefore determined whether individual or clusters of inflammatory mediators from a large biomarker panel were associated with ΔBP over 4.5 years, in young healthy adults.
We included 358 adults (white, n = 156; black, n = 202) with detailed information on ambulatory blood pressure (BP) at baseline and follow-up. Baseline blood samples were analysed for 22 inflammatory mediators using multiplexing technology. Principal component analysis was used to study associations between clusters of inflammatory mediators and ΔBP.
In the total cohort in multivariable-adjusted regression analyses, percentage change in 24hr systolic BP associated positively with Factors 1 (Interferon-gamma, interleukin (IL)-4, IL-7, IL-10, IL-12, IL-17A, IL-21, IL-23, macrophage inflammatory protein (MIP)-1α, MIP-1β, TNF-α, granulocyte-macrophage colony-stimulating factor (GM-CSF)) and 2 (IL-5, IL-6, IL-8, IL-13). Change in daytime systolic BP associated positively with Factors 1, 2 and 3 (C-Reactive protein, IL-1β, IL-2, MIP-3α). Subgroup analysis found these findings were limited to white study participants. Numerous associations were present between individual inflammatory mediators (Interferon-gamma, GM-CSF, IL-4, IL-6, IL-7, IL-8, IL-10, IL-12, IL-13, IL-17A, IL-21, IL-23, MIP-1α and MIP-1β) and ΔBP in the white but not black subgroups.
We found independent relationships between numerous inflammatory mediators (individual and clusters) and ΔBP over 4.5 years. The relationship between inflammatory markers and ΔBP was only found in white participants. ClinicalTrials.gov (Identifier: NCT03292094)..
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