title: Why are people with "poor lung function" at increased atherothrombotic risk? A critical review with potential therapeutic indications.
abstract: Patients classified as having a "poor lung function" in large populations studies are at increased risk of atherothrombosis, but potential mechanisms are unclear. A large proportion of these people are affected by chronic obstructive pulmonary disease (COPD), a recognized risk factor for vascular events. Systemic inflammation is the main atherothrombotic abnormality in COPD, but hypoxia-related platelet activation, pro-coagulant status and oxidative stress may play a role. Systemic inflammation is presumably a leading mechanism of atherothrombosis also in people who have a "restrictive" spirometric dysfunction, rather than the classic obstructive pattern of COPD. Many persons with "poor lung function" are affected by diabetes and their cardiovascular risk is therefore linked to the diabetic status. Patients affected by diabetes tend to have a "restrictive" dysfunction, rather than COPD. Recent studies show that restriction at spirometry precedes the onset of diabetes, thereby representing a marker of mechanisms involved in the pre-diabetic, insulin-resistant state. This is also proved by the fact that most patients with metabolic syndrome, a pre-diabetic condition, have a restrictive ventilatory pattern at spirometry. A significant proportion of people with "poor lung function" have visceral obesity, a cardiovascular risk factor. By hampering lung expansion, visceral obesity causes a restrictive ventilatory pattern. In conclusion, the term "poor lung function" includes various chronic illnesses with different mechanisms of atherothrombosis. Research is needed for better understanding why persons with lung dysfunctions have higher cardiovascular risk, and for identifying adequate preventive strategies.
authors.affiliation: Unit of Respiratory Diseases, Division of Internal Medicine, Leopoldo Parodi-Delfino Hospital, ASL Roma G, Colleferro (Rome), Italy. filippo.fimognari@virgilio.it
authors.forename: Filippo Luca
authors.initials: FL
authors.lastname: Fimognari
authors.forename: Simone
authors.initials: S
authors.lastname: Scarlata
authors.forename: Raffaele
authors.initials: R
authors.lastname: Antonelli-Incalzi
mesh_terms: D000318:Adrenergic beta-Agonists / Q000627:therapeutic use; D000818:Animals; D000893:Anti-Inflammatory Agents / Q000627:therapeutic use; D050197:Atherosclerosis / Q000150:complications* / Q000503:physiopathology; D001778:Blood Coagulation Disorders / Q000503:physiopathology; D001993:Bronchodilator Agents / Q000627:therapeutic use; D006801:Humans; D019161:Hydroxymethylglutaryl-CoA Reductase Inhibitors / Q000627:therapeutic use; D018836:Inflammation Mediators / Q000097:blood; D008171:Lung Diseases / Q000150:complications* / Q000188:drug therapy* / Q000503:physiopathology; D008659:Metabolic Diseases / Q000503:physiopathology; D009765:Obesity / Q000503:physiopathology; D018384:Oxidative Stress / Q000502:physiology; D015539:Platelet Activation / Q000502:physiology; D029424:Pulmonary Disease, Chronic Obstructive / Q000150:complications* / Q000188:drug therapy* / Q000503:physiopathology; D012307:Risk Factors; D013927:Thrombosis / Q000150:complications* / Q000503:physiopathology
chemical_list: D000318:Adrenergic beta-Agonists; D000893:Anti-Inflammatory Agents; D001993:Bronchodilator Agents; D019161:Hydroxymethylglutaryl-CoA Reductase Inhibitors; D018836:Inflammation Mediators