Burden of cardiovascular disease in Sub-Saharan Africa, 1990-2019: An analysis of the Global Burden of Disease Study.

INTRODUCTION: The rise in cardiovascular disease (CVD) in Sub-Saharan Africa (SSA) reflects a major shift from communicable to noncommunicable diseases as primary health challenges. Consequently, this study aims to explore the burden of CVD and associated risk factors in SSA using data from the Global Burden of Disease (GBD) database. METHODS: This study utilized data from the GBD 1990 to 2019 to examine CVD prevalence in 46 SSA countries. We employed Bayesian regression models, demographic techniques, and mortality-to-incidence ratios to analyze both prevalence and mortality rates. Additionally, disability-adjusted life years (DALYs) were computed, and various risk factors were examined using the GBD's comparative risk assessment framework. RESULTS: Between 1990 and 2019, CVD raw counts in SSA rose by 131.7 %, with a 2.1 % increase in age-standardized prevalence rates. The most prevalent conditions were ischemic heart disease, stroke, and rheumatic heart disease. During the same period, the age-standardized CVD deaths per 100,000 individuals decreased from 314 (1990) to 269 (2019), reflecting a -14.4 % decline. Age-standardized CVD DALY rates also showed a decrease from 6,755 in 1990 to 5,476 in 2019, with translates to 18.9 % reduction. By 2019, the Central African Republic, Madagascar, and Lesotho were the countries with the highest age-standardized DALY rates for all CVDs. CONCLUSIONS: The study highlights a contrasting trend in SSA's CVD landscape: a decrease in age-standardized mortality and DALYs contrasts with increasing CVD prevalence, emphasizing the need for targeted public health strategies that balance treatment advancements with intensified prevention and control measures.

Risk Factors for Unnecessary Antibiotic Prescribing for Acute Respiratory Tract Infections in Primary Care.

OBJECTIVE: To determine independent risk factors for inappropriate antibiotic prescribing for acute respiratory tract infections (ARIs) in internal medicine (IM) residency-based primary care offices. PATIENTS AND METHODS: A retrospective study was conducted to measure antibiotic prescribing rates, and multivariable analysis was utilized to identify predictors of inappropriate prescribing among patients presenting to IM residency-based primary care office practices. Patients with an office visit at either of 2 IM residency-based primary care office practices from January 1, 2016, through December 31, 2016, with a primary encounter diagnosis of ARI were included. RESULTS: During the study period, 911 unique patient encounters were included with 518 for conditions for which antibiotics were considered always inappropriate. Antibiotics were not indicated in 85.8% (782 of 911) of encounters. However, antibiotics were prescribed in 28.4% (222 of 782) of these encounters. Inappropriate antibiotic prescribing occurred in 111 of 518 (21.4%) encounters for conditions for which antibiotics are always inappropriate. Using multivariable logistic regression analysis to assess for independent risk factors when adjusted for other potential risk factors for office visits at which antibiotics were not indicated, IM resident-associated visits (odds ratio, 0.25; 95% CI, 0.18-0.36) was the only variable independently associated with lower risk of inappropriate antibiotic prescribing. CONCLUSION: For ARI visits at which antibiotics were not indicated, IM resident comanagement was associated with lower rates of inappropriate prescribing.

Silent aortic dissection presenting as transient locked-in syndrome.

Acute aortic dissection is a medical emergency. Without prompt recognition and treatment, the mortality rate is high. An atypical presentation makes timely diagnosis difficult, especially if the patient is experiencing no characteristic pain. Many patients with aortic dissection are reported to have presented with various neurologic manifestations, but none with only a presentation of transient locked-in syndrome.Herein, we report a case of completely painless aortic dissection in a woman who presented with a transient episode of anarthria, quadriplegia, and preserved consciousness. On physical examination, she had a 40-point difference in blood pressure between her left and right arms, and a loud diastolic murmur. The diagnosis of acute aortic dissection was reached via a combination of radiography, computed tomography, echocardiography, and a high index of clinical suspicion. The patient underwent emergency surgery and ultimately experienced a successful outcome.To our knowledge, this is the 1st report of aortic dissection that presented solely as locked-in syndrome. We suggest that silent aortic dissection be added to the differential diagnosis for transient locked-in syndrome.

Effects of post-injury hypothermia and nerve growth factor infusion on antioxidant enzyme activity in the rat: implications for clinical therapies.

The pathological sequelae of traumatic brain injury (TBI) include increased oxidative stress due to the production of reactive oxygen species (ROS). Regulation of ROS levels following TBI is determined primarily by antioxidant enzyme activity that in turn can be influenced by nerve growth factor (NGF). Hypothermia is one of the current therapies designed to combat the deleterious effects of TBI. However, it has been shown to suppress post-trauma increases in NGF levels in rat brain. The present study sought to determine whether post-injury hypothermia also impairs the antioxidant response to injury, and if such an effect could be reversed by infusion of exogenous NGF. We employed a lateral controlled cortical impact injury model in rat, followed by moderate hypothermia treatment with supplemental intracerebroventricular infusion of NGF or vehicle. The time course of changes in post-injury/intervention levels of NGF and activity of three major enzymes responsible for ROS scavenging, catalase (CAT), glutathione peroxidase (GPx) and superoxide dismutase (SOD), was determined in the hippocampus. Relative to levels in injured, normothermic animals, hypothermia treatment not only suppressed NGF levels, but also attenuated CAT and GPx activity, and increased SOD activity. Infusion of NGF in injured, hypothermia-treated animals was ineffective in restoring hippocampal antioxidant enzymes activity to levels produced after injury under normothermic conditions, although it was able to increase septal cholinergic (choline acetyltransferase) enzyme activity. These results have implications for clinical treatment of TBI, demonstrating that moderate hypothermia suppresses NGF and the antioxidant response after TBI; the latter cannot be countered by exogenous NGF administration.

Time course analysis of hippocampal nerve growth factor and antioxidant enzyme activity following lateral controlled cortical impact brain injury in the rat.

Gradual secondary injury processes, including the release of toxic reactive oxygen species, are important components of the pathogenesis of traumatic brain injury (TBI). The extent of oxidative stress is determined in part by the effectiveness of the antioxidant response, involving the enzymes glutathione peroxidase (GPx), catalase (CAT), and superoxide dismutase (SOD). Since nerve growth factor (NGF) may be involved in the initiation of antioxidant activity, we employed a controlled cortical impact injury model in rats to produce secondary hippocampal damage and determined the subsequent time course of changes in NGF production and GPx, CAT, and SOD activity in this brain region. Hippocampal NGF production showed a rapid increase with a biphasic response after TBI. NGF protein was increased at 6 h, plateaued at 12 h, declined by 7 days, and exhibited a second rise at 14 days after injury. Similar to NGF, hippocampal GPx activity also showed a biphasic response, increasing by 12 h, declining at 24 h, and exhibiting a second peak at 7 days. In contrast, increased CAT activity occured steadily from 1 day through 7 days after injury. SOD activity was decreased at 6 h after injury, and continued to decline through 14 days. The initial rise in NGF preceded that of CAT, and coincided with an increase in GPX and a drop in SOD activity. These data demonstrate a complex temporal spectrum of antioxidant enzyme activation following secondary brain injury in the hippocampus, and suggest a selective regulatory role for NGF in this response.