Anticoagulant agents are widely used in the treatment of thromboembolic events and in stroke prevention. Data about their effects on bone tissue are in some cases limited or inconsistent (oral anti-vitamin K agents), and in others are sufficiently strong (heparins) to suggest caution in their use in subjects at risk of osteoporosis. This review analyses the effects of this group of drugs on bone metabolism, on bone mineral density, and on fragility fractures. A literature search strategy was developed by an experienced team of specialists by consulting the MEDLINE platform, including published papers and reviews updated to March 2019. Literature supports a detrimental effect of heparin on bone, with an increase in fracture rate. Low molecular weight heparins (LMWHs) seem to be safer than heparin. Although anti-vitamin K agents (VKAs) have a significant impact on bone metabolism, and in particular, on osteocalcin, data on bone mineral density (BMD) and fractures are contrasting. To date, the new direct oral anticoagulants (DOACs) are found to safe for bone health.

Hemodynamic dysfunction mainly characterizes pathophysiology of peripheral arterial disease (PAD) leading to chronic ischemia. Hemodynamic dysfunction is the origin of intermittent claudication (chronic PAD) or of critical limb ischemia (very severe PAD). Notably, it is well known that oxidative stress (OxS) plays a pathophysiological role in PAD. The higher production of reactive oxygen species (ROS) from OxS and reduced redox capability are two crucial players in initiating and progressing PAD. A number of biomarkers highlight OxS and monitor it in PAD. The present review summarizes data on OxS, on biomarkers available to mark OxS occurrence and to monitor on PAD progression, as well as to evaluate the effects treatments in PAD patients. In conclusion, by detailing OxS and its biomarkers, we hope to encourage more studies to focus on drugs which combat OxS and inflammation.

Peripheral arterial disease (PAD) is an atherosclerotic disease that affects a wide range of the world’s population, reaching up to 200 million individuals worldwide. PAD particularly affects elderly individuals (>65 years old). PAD is often underdiagnosed or underestimated, although specificity in diagnosis is shown by an ankle/brachial approach, and the high cardiovascular event risk that affected the PAD patients. A number of pathophysiologic pathways operate in chronic arterial ischemia of lower limbs, giving the possibility to improve therapeutic strategies and the outcome of patients. This review aims to provide a well detailed description of such fundamental issues as physical exercise, biochemistry of physical exercise, skeletal muscle in PAD, heme oxygenase 1 (HO-1) in PAD, and antioxidants in PAD. These issues are closely related to the oxidative stress in PAD. We want to draw attention to the pathophysiologic pathways that are considered to be beneficial in order to achieve more effective options to treat PAD patients.

Peripheral arterial disease (PAD) affects individuals particularly over 65 years old in the more advanced countries. Hemodynamic, inflammatory, and oxidative mechanisms interact in the pathophysiological scenario of this chronic arterial disease. We discuss the hemodynamic, muscle tissue, and oxidative stress (OxS) conditions related to chronic ischemia of the peripheral arteries. This review summarizes the results of evaluating both metabolic and oxidative markers, and also therapy to counteract OxS. In conclusion, we believe different pathways should be highlighted to discover new drugs to treat patients suffering from PAD.

Peripheral arterial disease (PAD) is an atherosclerotic disease closely associated with high morbidity and mortality in cardiac events. Inflammation is crucial in atherosclerosis both at triggering and in progression. Numerous inflammatory biomarkers (cytokines, matrix metalloproteinases (MMPs), selectin, intracellular adhesion molecule (ICAM), vascular cell adhesion molecule (VCAM) C-reactive protein (CRP), fibrinogen) have been measured in atherosclerotic diseases including PAD. This paper summarizes the data on the inflammatory biomarkers for PAD pathophysiology and highlights the most useful markers in monitoring PAD outcomes.