Table 1.

Pathophysiology of risk factors for CVD, COPD, and MACEs.

Risk factors	Pathophysiology
Acute exacerbation of COPD	Multifactorial (viruses, bacteria, smoking, air pollution, GERD)
	Initiates the inflammatory milieu
	Atheromatous plaque destabilization
	Induces arterial stiffness and myocardial inflammation
Smoking	COPD progression and exacerbation
	Atheromatous plaque initiation, progression, and destabilization
	Diminishes transcription factor FOXP3 with role in T cell development
	Reduces cilia, stimulates macrophages
	Promotes the hypercoagulation state, activates plateles
	Accentuates endothelial dysfunction
	Increases ox-LDL
	May also have anti-inflammatory effect
Air pollution	Atheromatous plaque initiation, progression, and destabilization
	Contibutes to COPD progression and exacerbation
	Increases inflammation
Hyperlipidemia	Atheromatous plaque initiation, progression, and destabilization
	Ox-LDL activates transcription factors involved in COPD pathogenesis
	Ox-LDL increases chemotaxis of neutrophils, eosinophils, and monocytes
	Ox-LDL increases pro-inflammatory cytokines
	OxLDL increases ROS production
Diabetes mellitus	Increases systemic inflammation and oxidative stress
	May cause direct damage by hyperglycemia
	Involved in myocelular hypertrophy and fibrosis
Hypertension	Induces structural alterations of the left ventricle and atrium
	Induces vascular system alterations
	Atheromatous plaque progression
	Increases ROS via NADPH oxidase stimulated by angiotensin II

COPD, chronic obstructive disease; GERD, gastroesophageal reflux disease; Ox-LDL, oxidized low-density lipoprotein; ROS, radical oxygen species.