Clustering is the unsupervised classification of patterns (observations, data items, or feature vectors) into groups (clusters). The clustering problem has been addressed in many contexts and by researchers in many disciplines; this reflects its broad appeal and usefulness as one of the steps in exploratory data analysis. However, clustering is a difficult problem combinatorially, and differences in assumptions and contexts in different communities has made the transfer of useful generic concepts and methodologies slow to occur. This paper presents an overview of pattern clustering methods from a statistical pattern recognition perspective, with a goal of providing useful advice and references to fundamental concepts accessible to the broad community of clustering practitioners. We present a taxonomy of clustering techniques, and identify cross-cutting themes and recent advances. We also describe some important applications of clustering algorithms such as image segmentation, object recognition, and information retrieval.

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Data clustering: a review

2016 ESC Guidelines for the diagnosis and treatment of acute and chronic heart failure: The Task Force for the diagnosis and treatment of acute and chronic heart failure of the European Society of Cardiology (ESC). Developed with the special contribution of the Heart Failure Association (HFA) of the ESC.

https://caltcm.memberclicks.net/assets/documents/acc_aha_chf_2013_guidelines.pdf

2013 ACCF/AHA Guideline for the Management of Heart Failure: A Report of the American College of Cardiology Foundation/American Heart Association Task Force on Practice Guidelines

Atherosclerosis, the principal cause of heart attack, stroke and gangrene of the extremities, is responsible for 50% of all mortality in the USA, Europe and Japan. The lesions result from an excessive, inflammatory-fibroproliferative response to various forms of insult to the endothelium and smooth muscle of the artery wall. A large number of growth factors, cytokines and vasoregulatory molecules participate in this process. Our ability to control the expression of genes encoding these molecules and to target specific cell types provides opportunities to develop new diagnostic and therapeutic agents to induce the regression of the lesions and, possibly, to prevent their formation.

The pathogenesis of atherosclerosis: a perspective for the 1990s

The Adult Treatment Panel III (ATP III) of the National Cholesterol Education Program issued an evidence-based set of guidelines on cholesterol management in 2001. Since the publication of ATP III, 5 major clinical trials of statin therapy with clinical end points have been published. These trials addressed issues that were not examined in previous clinical trials of cholesterol-lowering therapy. The present document reviews the results of these recent trials and assesses their implications for cholesterol management. Therapeutic lifestyle changes (TLC) remain an essential modality in clinical management. The trials confirm the benefit of cholesterol-lowering therapy in high-risk patients and support the ATP III treatment goal of low-density lipoprotein cholesterol (LDL-C) <100 mg/dL. They support the inclusion of patients with diabetes in the high-risk category and confirm the benefits of LDL-lowering therapy in these patients. They further confirm that older persons benefit from therapeutic lowering of LDL-C. The major recommendations for modifications to footnote the ATP III treatment algorithm are the following. In high-risk persons, the recommended LDL-C goal is <100 mg/dL, but when risk is very high, an LDL-C goal of <70 mg/dL is a therapeutic option, ie, a reasonable clinical strategy, on the basis of available clinical trial evidence. This therapeutic option extends also to patients at very high risk who have a baseline LDL-C <100 mg/dL. Moreover, when a high-risk patient has high triglycerides or low high-density lipoprotein cholesterol (HDL-C), consideration can be given to combining a fibrate or nicotinic acid with an LDL-lowering drug. For moderately high-risk persons (2+ risk factors and 10-year risk 10% to 20%), the recommended LDL-C goal is <130 mg/dL, but an LDL-C goal <100 mg/dL is a therapeutic option on the basis of recent trial evidence. The latter option extends also to moderately high-risk persons with a baseline LDL-C of 100 to 129 mg/dL. When LDL-lowering drug therapy is employed in high-risk or moderately high-risk persons, it is advised that intensity of therapy be sufficient to achieve at least a 30% to 40% reduction in LDL-C levels. Moreover, any person at high risk or moderately high risk who has lifestyle-related risk factors (eg, obesity, physical inactivity, elevated triglycerides, low HDL-C, or metabolic syndrome) is a candidate for TLC to modify these risk factors regardless of LDL-C level. Finally, for people in lower-risk categories, recent clinical trials do not modify the goals and cutpoints of therapy.

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Implications of Recent Clinical Trials for the National Cholesterol Education Program Adult Treatment Panel III Guidelines

The development of antiarrhythmic drugs.

Background. Dothebenefits ofintensive lipid-lowering therapy seeninsymptomatic patients extend to high-risk subjects whohaveneverhadsymptoms? Methods andResuls. Of120men completing theFATStrial, 91weresymptomatic and29asymptomatic. Allhadapolipoprotein B 2125mg/dL, a positive family history, andcoronaryatherosclerosis. Allwere counseled indiet andrandomized tointensive therapy: colestipol 10gTIDpluseither niacin 1gQIDor lovastatin 20mg BIDor toconventional therapy: placebos, or colestipol iflow-density lipoprotein cholesterol was elevated. Endpoints included quantitative arteriographic disease change andclinical events overa2.5-year interval. Atbaseline, symptomatic andasymptomatic patients hadcomparable risk profiles, butproximal stenosis severity averaged 36%forsymptomatic and23%forasymptomatic patients (P<.001). Amongthe91symptomatic patients, those intheintensive groupexperienced definite (.101%S) proximal lesion progression less frequently thanconventional (24%ofintensive versus48%ofconventional) anddefinite regression more frequently (36%ofintensive versus15%ofconventional) (P=.009). Similarly, among the29asymptomatic patients, 19%ofintensive versus38%ofconventional had progression and31%ofintensive versus0%1 ofconventional, regression (P=.04). Ischemia on baseline exercise tolerance testing was associated withsignificantly greater proximal disease progression among theasymptomatic patients. Clinical cardiovascular events(death, infarction, or revascularization) occurred in10of38symptomatic patients originally assigned toconventional therapy, compared with5 of76symptomatic patients assigned tointensive (P<.01); no asymptomatic patient hadan event. Concluions. Asymptomatic subjects withthishigh-risk profile haveless coronarydisease atbaseline thancomparable symptomatic patients, andtheyhavean excellent short-term clinical prognosis. However, asymptomatic subjects areindistinguishabl e fromsymptomatic patients intermsoftheir arterial disease progression withconventional therapy andtheir regression withintensive. Thesefindings may justify an active treatment strategy insuchsubjects, particularly those withprovokable ischemia. (Circulation. 1993;88:2744-2753.)

Lloyd D. Fisher

Papers

The development of antiarrhythmic drugs.

Effects ofIntensive Lipid-Lowering Therapy on theCoronary Arteries ofAsymptomatic Subjects WithElevated Apolipoprotein B

Statistical issues and analysis of mortality and morbidity randomized clinical trials in congestive heart failure

Ethics of Randomized Trials

in coronary artery surgery (CASS). Clinical and angiographic predictors of operative mortality from the collaborative study