Revascularization Strategies in Patients with Coronary Artery Disease and Chronic Obstructive Lung Disease.

Purpose of review: This paper assesses recent literature on the impact of chronic obstructive pulmonary disease (COPD) in patients with coronary artery disease (CAD) undergoing revascularization. Specifically, to determine if there is an optimal revascularization strategy for this patient population, and if there are other modalities to assess the risks. Recent findings: There are limited new data in the last year addressing this clinical question. Recently there have been a series of studies which reinforced that COPD is a key independent risk factor for adverse outcomes after revascularization. There is no optimal revascularization strategy; however, there was a nonsignificant signal of potential benefit with percutaneous coronary intervention (PCI) with short-term outcomes in the SYNTAXES trial. Currently, pulmonary function tests (PFT) are limited in clarifying risk assessments prior to revascularization, and there are investigations into the use of biomarkers to provide further insight into this increased risk of adverse outcomes in patients with COPD. Summary: COPD is a key risk factor for poor outcomes in patients requiring revascularization. More investigations are needed to determine the optimum revascularization strategy.

Approach to the Patient with Cough.

Cough is a common presenting symptom for patients in a primary care setting. Chronic cough is defined as a cough lasting for more than 8 weeks. The most common causes of chronic cough are upper airway cough syndrome, asthma, and gastroesophageal reflux disease. Detailed history and physical examination are critical in identifying potential etiologies of cough. When there is no prevailing diagnosis, step-wise empiric trial of medication is a strategic and cost-effective approach. Certain features of chronic cough should provoke an expedited and invasive diagnostic strategy. Effectively treating patients with chronic cough has a high impact on quality of life.

Faculty development in point of care ultrasound for internists.

Lack of general medicine faculty expertise is a likely contributor to the slow adoption of point of care ultrasound (POCUS) by internal medicine (IM) residency training programs. We developed a 10-week faculty development program, during which 15 faculty members participated in 2 hours and 10 hours of online didactic and hands-on training, respectively. Pre-post comparisons showed that there were statistically significant improvements in faculty participants' ability to interpret images (p<0.001), perceived understanding of the capabilities and limitations of POCUS (p=0.003), comfort using POCUS to make clinical decisions (p=0.003), and perceptions regarding the extent to which POCUS can improve patient care (p=0.026). The next challenge for IM programs is to improve access to ultrasound machines and provide follow-up workshops to facilitate further development of skills and integration of POCUS into daily practice by general medicine faculty.

Circulating endothelial microparticles as a measure of early lung destruction in cigarette smokers.

RATIONALE: There is increasing evidence that emphysema is associated with primary loss of pulmonary capillary endothelium. Plasma levels of endothelial microparticles (EMPs), small vesicles released from activated or apoptotic endothelial cells, are elevated in vascular-related disorders. OBJECTIVES: To evaluate whether plasma EMP levels are elevated in smokers with early lung destruction as assessed by normal spirometry but reduced diffusing capacity of the lung for carbon monoxide (Dl(co)). METHODS: Lung health was assessed by pulmonary function tests (PFTs: spirometry, total lung capacity, Dl(co)) and chest X-ray; smoking status was assessed by urine nicotine and cotinine. EMP levels (CD42b(-)CD31(+) microparticles) were quantified as activated or apoptotic. The initial cohort (n = 92) included healthy nonsmokers (normal PFTs), healthy smokers (normal PFTs), and smokers with early evidence of lung destruction (normal spirometry, low Dl(co)). Two prospective cohorts were then tested: a group similar to the initial cohort and an HIV1(+) cohort. MEASUREMENTS AND MAIN RESULTS: Healthy smokers had mildly increased levels of EMPs. Strikingly, 95% of smokers with normal spirometry, low Dl(co) had increased EMPs, with reduced CD62(+)/CD31(+) ratios (P < 10(-4)) and elevated CD42b(-)CD31(+) annexin V(+) EMPs (P < 10(-4)), suggesting derivation from endothelial apoptosis. Most elevated EMPs were angiotensin-converting enzyme positive, suggesting derivation from pulmonary capillaries. Both prospective cohorts confirmed the initial cohort data. CONCLUSIONS: Plasma EMPs with apoptotic characteristics are elevated in smokers with normal spirometry but reduced Dl(co), consistent with the concept that emphysema is associated, in part, with capillary endothelium apoptosis, suggesting that the early development of emphysema might be monitored with plasma EMP levels.

An anticonvulsant profile of the ketogenic diet in the rat.

The present study was designed to evaluate the anticonvulsant effects of a high-fat ketogenic diet (KD) in rats. Animals were maintained on one of four experimental diets: (1) calorie-restricted ketogenic (KCR); (2) calorie-restricted normal (NCR); (3) ad libitum ketogenic (KAL); or (4) ad libitum normal (NAL). The calorie-restricted diets were fed in quantities such that they were calorically equivalent. All animals began diet treatment at age P37 and each was subjected to one of five chemically-induced seizure tests: bicuculline (BIC; s.c.), picrotoxin (PIC; s.c.), kainate (KA, i.p. or s.c.) and gamma-butyrolactone (GBL, i.p.), strychnine (s.c.). Bipolar epidural electrodes were implanted under ketamine/xylazine anesthesia to permit recording the spike and wave discharges (SWD) characteristic of electroencephalograms during absence seizures. Ketonemia was assayed by measuring blood levels of beta-hydroxybutyrate (BHB) spectrophotometrically prior to induction of seizures in each experiment. Animals fed ketogenic diets (i.e. either calorie restricted or ad libitum) exhibited greater blood levels of BHB compared to control groups. Seizure results show that treatment with a KD: (1) reduced the incidence of bicuculline-induced convulsions; (2) diminished the number of picrotoxin-induced seizures (KCR group only); (3) increased latency to GBL-induced SWD and reduced both the number and duration of SWD; but (4) conferred no protection from strychnine-induced seizures; and (5) made KA-induced seizures more severe. Together these results indicate a spectrum of anticonvulsant action for the KD in rats that includes threshold seizures induced via GABA receptors (BIC, PIC, GBL) but not those induced at glycine (strychnine) or the KA-subclass of glutamate receptors. Uniquely, the KD is the only treatment described that protects against both convulsive and non-convulsive (absence) seizures in rats.