The Canadian Cardiovascular Society grading of angina pectoris revisited 30 years later

BACKGROUND: The Canadian Cardiovascular Society (CCS) grading of angina pectoris was described in the medical literature in 1976. OBJECTIVES: To describe the origin of this grading, its worldwide acceptance, critiques, perceived limitations and alternative systems. METHODS: The present author, who chaired the CCS ad hoc committee that developed this grading system in 1972, used documentation based on personal correspondence, and information from medline and international citation indexes searches. RESULTS: The CCS committee's mandate was to standardize the definition of terms used in reporting studies of coronary artery disease and coronary artery bypass graft surgery. The committee defined a four-level system modelled on the New York Heart Association functional classification of patients with diseases of the heart, and the American Medical Association classes of organic heart diseases. Threshold activities that produced angina were detailed to assess reliably the severity of exertional angina by independent observers, and changes over time. The grading system has been cited over 650 times in the literature since its official publication in 1976. Although this grading system was found to be generally relevant and practical, several imperfections and potential limitations were reported, the most pertinent being the criterion "anginal syndrome may be present at rest" included in grade IV, which was found to be inappropriate and confusing. The prognostic significance of the grading system, despite the finding that this was not its primary goal, was also thought to be inadequate. CONCLUSION: Although this grading system of the severity of effort angina has been accepted throughout the world over the past 30 years, a revision is desirable considering its potential imperfections and inconsistencies with present day management of ischemic heart disease.     

Inhibitory effect of melatonin on homocysteine-induced lipid peroxidation in rat brain homogenates

Oxidative damage is implicated in several pathologies including cardiovascular disease. As a model system to study the response of cells to oxidative insults, homocysteine toxicity was examined since it is an independent risk factor for atherosclerotic disease. The levels of malondialdehyde and 4-hydroxyalkenals were assayed as an index of oxidatively damaged lipid. In in vitro experiments, the increase of lipid peroxidation products induced by homocysteine were concentration- and time-dependent. To study the protective effect of melatonin on homocystine induced lipid peroxidation, brain homogenates were treated with different concentrations of melatonin. The accumulation of malondialdehyde and 4-hydroxyalkenals induced by homocysteine was significantly reduced by melatonin in a concentration-dependent manner. Additionally, a melatonin concentration of 1.5 mM reduced the levels of oxidatively damaged lipid products below those measured in control homogenates (no homocysteine, no melatonin). These data suggest that melatonin, an endogenous antioxidant may have a role in protecting cells from oxidative damage due to homocysteine and they support the idea that pharmacological concentrations could be used as a therapeutic agent in reducing cardiovascular disease where homocysteine may be a causative or contributing agent.     

Postoperative spondylodiskitis due to Stomatococcus mucilaginosus in an immunocompetent patient

A case is reported of postoperative spondylodiskitis due to Stomatococcus mucilaginosus in an immunocompetent woman. The route of infection remains unknown. Intravenous treatment with cefotaxime and fosfomycin was given, followed by oral administration of rifampin and pristinamycin until resolution of infection. This report shows that this bacterium can cause severe infections in immunocompetent patients.     

VALsartan In Acute myocardial iNfarcTion (VALIANT) trial: baseline characteristics in context

BACKGROUND: The VALsartan In Acute myocardial iNfarcTion (VALIANT) trial compared outcomes with: (1) angiotensin-converting enzyme inhibition (ACEI) with the reference agent captopril; (2) angiotensin-receptor blockade (ARB) with valsartan; or (3) both in patients with heart failure (HF) and/or left ventricular systolic dysfunction (LVSD) after myocardial infarction (MI). AIMS: a goal of this active-control trial was to simulate conditions that would lead current practitioners to use ACEIs. Thus, we compared characteristics of VALIANT patients with those of patients in placebo-controlled trials that established ACEIs as standard treatment. METHODS AND RESULTS: We collected demographic, clinical, medication and imaging information from 14703 patients in 24 countries. This high-risk population was a median 65.8 years old, and 31.1% were female. Most (51.8%) showed imaging evidence of LVSD at enrollment. Most (72%) had Killip class>/=II HF. Patients received evidence-based therapies at rates similar to those of contemporary MI trials and at an improved rate compared with prior placebo-controlled ACEI trials. CONCLUSION: VALIANT represents the largest globally representative cohort enrolled with HF and/or LVSD after MI. Patients were similar to those in placebo-controlled ACEI trials while reflecting improvements in evidence-based care. With enrollment complete, VALIANT is poised to define the optimal strategy for renin-angiotensin system blockade after MI to improve cardiovascular outcomes.     

Rapid modulation of GABA in sensorimotor cortex induced by acute deafferentation

Recovery of function after acute injury to the central nervous system may be controlled by the availability of gamma-aminobutyric acid (GABA), the main inhibitory neurotransmitter in the cerebral cortex. Acute lesions as well as manipulation of sensory inputs can lead to rapid reorganization of the cerebral cortex, occurring within minutes to hours. Reduction of cortical inhibitory tone through a decrease in the availability of GABA has been suggested as a possible mechanism; however, the degree and temporal course of the changes in brain GABA are not known. A novel method using two-dimensional J-resolved magnetic resonance spectroscopy showed that GABA levels in the human sensorimotor cortex are quickly reduced within minutes of deafferentation. This finding strongly supports the view that the release of latent corticocortical projections from tonic inhibition through decreased GABA availability is a mechanism of rapid cortical plasticity. Reduction of brain GABA can play a pivotal role in regulating the extent of rapid cortical reorganization after lesions or changes in sensory input.     

Biliary-enteric transanastomotic stenting with Intestofix

Background: Biliary‐enteric transanastomotic stenting is useful under adverse local conditions or when small‐calibre bile ducts are encountered. Methods: A commercially available feeding jejunostomy kit, Intestofix, was inserted transjejunally through the blind loop of a Roux‐en‐Y hepatico‐jejunostomy. Conclusions: The stent splinted the anastomosis to reduce biliary leaks and may help to prevent subsequent stricture formation.     

Spiral CT quantification of aorto-renal calcification and its use in the detection of atheromatous renal artery stenosis: A study in 42 patients

Purpose: To investigate whether a correlation exists between aortic and renal arterial calcifications detected with spiral CT and significant angiographic renal artery stenosis (RAS). Methods: Forty-two patients (mean age 67 years, range 37–84 years), of whom 24 were hypertensive, prospectively underwent abdominal helical CT and aortic and renal arteriography. The 3-mm thickness CT scans (pitch = 1) were reconstructed each millimeter. A manual outline of the renal artery including its ostial portion was produced. Calcific hyperdensities were defined as areas of density more than 130 HU. CT data were compared with the presence or absence of RAS on angiography (24 cases); hypertension and age were taken into account (Mann-Whitney U-test). Results: CT detection and quantification appeared to be reliable and reproductible. We did not find any correlation between aortic and renal arterial calcifications and RAS, even for the patients above 65 years, with or without hypertension. There was no correlation either between calcifications and hypertension in patients without RAS. Conclusion: In this population, aortic and renal arterial calcifications have no predictive value for RAS.