Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0002962 (angina)
 21,142 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

There is an established inverse relationship between the regular light consumption of alcohol (5-10 g/day) and the incidence of coronary artery disease (CAD). This association has several biologically plausible mechanisms with dose-dependent effects of alcohol to increase HDL cholesterol, lower plasma fibrinogen and inhibit platelet aggregation. However, such a protective effect against atheroma cannot be considered in isolation from known adverse effects on blood pressure and triglycerides or possible detrimental effects of episodic or binge drinking on several other cardiovascular end-points and risk factors. In subjects with pre-existing CAD, an alcoholic binge can increase both silent myocardial ischaemia and angina. During withdrawal following binge drinking, marked fluctuations in blood pressure together with heightened platelet activation and adverse changes in the balance of fibrinolytic factors, may offer an explanation for the reported association between episodic heavy drinking and ischaemic stroke. This has been seen particularly in young males and extends further to an increase in both subarachnoid haemorrhage and intracerebral haemorrhage after binge drinking. Intervention studies in man have shown acute increases in blood pressure in men who drink predominantly at weekends, compared to longer-term pressor effects in regular daily drinkers. We have been unable, however, to reproduce the finding of unfavourable effects of binge drinking on the lipid profile that have been reported in animal studies and man. Binge drinking may also induce cerebrovascular spasm or cause both ventricular and supraventricular arrhythmias, especially atrial fibrillation. Alcohol-induced arrhythmia has been postulated as the basis for alcohol-related sudden coronary death in those subjects with pre-existing CAD. Hence, further exploration of any protective association of alcohol against CAD needs to carefully consider the implications of pattern of drinking for the relationship. The modulating influences of co-timing of drinking with meals, cigarette smoking or illicit drug use also need to be evaluated. Without such vital information, public health advice on alcohol and CAD will be limited in its scope and potentially flawed in its impact.
Addiction 1999 May
PMID:Influence of pattern of drinking on cardiovascular disease and cardiovascular risk factors--a review. 1056 30

Cigarette smoking kills about six million smokers per year worldwide, and the cigarette has become a symbol of threat to mankind, particularly in industrialized countries. Tobacco smoking causes signs of addiction due to nicotine, but it is the inhaled and exhaled smoke that causes damage to health if cigarette smoking is continued for one or more decades. It is very difficult to attain a high efficacy of stopping smoking using methods of primary prevention in children and young adults. Secondary and tertiary prevention methods use medical and psychological support to the smoker (behavioural and aversion therapy) as well as medical advice in combination with drugs such as nicotine replacement or bupropion. Using a combination of these methods can increase effectiveness up to 45%. Use of nicotine replacement therapy (NRT) in combination with medical advice is the method of smoking cessation recommended by the World Health Organization. Bupropion causes several severe side effects which are not observed with NRT. This article reviews various NRT formulations, including chewing gum, patch, nasal spray, tablet and inhaler, and our experience of using NRT in medical practice, such as adverse events, withdrawal symptoms and the efficacy of NRT in patients with coronary heart disease (angina pectoris, cardiac arrhythmias, etc.), are briefly mentioned. Overall, we need greater efforts in practising primary and secondary prevention among current and future physicians to solve the health problems associated with tobacco use in many nations.
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PMID:What can we do in secondary prevention of cigarette smoking? 1467 72

Background Spinal cord stimulation (SCS) is a surgical treatment for chronic neuropathic pain refractory to conventional treatment. SCS treatment consists of one or more leads implanted in the epidural space of the spinal canal, connected to an implantable pulse generator (IPG). Each lead carries a number of contacts capable of delivering a weak electrical current to the spinal cord, evoking a feeling of peripheral paresthesia. With correct indication and if implanted by an experienced implanter, success rates generally are in the range of about 50-75%. Common indications include complex regional pain syndrome (CRPS I), angina pectoris, and radicular pain after failed back surgery syndrome, and the treatment is also used to treat stump pain after amputation, and pain due to peripheral nerve injury, peripheral vascular disease, and diabetic neuropathy. Recommended contraindications for the treatment include pregnancy, coagulopathy, severe addiction to psychoactive substances, and lack of ability to cooperate (e.g. due to active psychosis or cognitive impairment). Most common complications to the treatment include lead migration, lead breakage, infection, pain over the implant, and dural puncture. Despite extensive research in the area, the mechanisms of action are still only partially understood. Methods In this topical review the historical background behind the treatment is described and the current theories on the mechanism of action are presented. The implantation procedure is described in detail and illustrated with a series of intraoperative pictures. Finally, indications for SCS are discussed along with some of the controversies surrounding the therapy. Implications The reader is presented with a broad overview of spinal cord stimulation, including the historical and theoretical background, practical implantation technique, and clinical application.
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PMID:Spinal cord stimulation: Background and clinical application. 2991 13

The L-type calcium channel blocker fendiline has been shown to interfere with Ras-dependent signaling in K-Ras mutant cancer cells. Earlier studies from our lab had shown that treatment of pancreatic cancer cells with fendiline causes significant cytotoxicity and interferes with proliferation, survival, migration, invasion and anchorage independent growth. Currently there are no effective therapies to manage PDACs. As fendiline has been approved for treatment of patients with angina, we hypothesized that, if proven effective, combinatorial therapies using this agent would be easily translatable to clinic for testing in PDAC patients. Here we tested combinations of fendiline with gemcitabine, visudyne (a YAP1 inhibitor) or tivantinib (ARQ197, a c-Met inhibitor) for their effectiveness in overcoming growth and oncogenic characteristics of PDAC cells. The Hippo pathway component YAP1 has been shown to bypass K-Ras addiction, and allow tumor growth, in a Ras-null mouse model. Similarly, c-Met expression has been associated with poor prognosis and metastasis in PDAC patients. Our results presented here show that combinations of fendiline with these inhibitors show enhanced anti-tumor activity in Panc1, MiaPaCa2 and CD18/HPAF PDAC cells, as evident from the reduced viability, migration, anchorage-independent growth and self-renewal. Biochemical analysis shows that these agents interfere with various signaling cascades such as the activation of Akt and ERK, as well as the expression of c-Myc and CD44 that are altered in PDACs. These results imply that inclusion of fendiline may improve the efficacy of various chemotherapeutic agents that could potentially benefit PDAC patients.
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PMID:Fendiline Enhances the Cytotoxic Effects of Therapeutic Agents on PDAC Cells by Inhibiting Tumor-Promoting Signaling Events: A Potential Strategy to Combat PDAC. 3110 Aug 13

Cardiovascular disease (CVD) is a common cause of death, representing 29% of the mortality all over the word. Estimates for 2006 show that CVD is one of the world's main cause of death, with 17.1 million death per year. More than 70 million Americans have been diagnosed with various forms of CVD, including high blood pressure, coronary artery disease (acute myocardial infarction and angina pectoris), disorders of peripheral arteries etc. There is strong evidence that periodontal disease (PD) is associated with an increased risk of CVD. In addiction many patients with CVD are also affected by PD, which can be mild or severe. The aim of this manuscript is to investigate the effects of periodontal therapy on the management of CVD. 34 randomised controlled trials and reviews were included in this manuscript to test the effects of different periodontal therapies for patients with CVD. In conclusion, we may affirm that there is some lack of knowledge on relations between PD and CVD, however there is sufficient evidence to justify a periodontal treatment to prevent CVD, in fact PD is very prevalent in middle-aged population and can have a significant impact on the cardiovascular function.
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PMID:Why patients with cardiovascular risks go to dentists. Is there sufficient evidence of influence of periodontal therapy on cardiovascular disease? 3153 57