Cardiovascular damage from steroids

Parameters of left and right ventricular function and LGE burden were measured in 205 patients with left ventricular ejection fraction >50% and extracardiac sarcoidosis who underwent cardiovascular magnetic resonance for LGE evaluation. The association between covariates and death/VT in the entire group and within the LGE+ group was determined using Cox proportional hazard models and time-dependent receiver-operator curves analysis. Forty-one of 205 patients (20%) had LGE; 12 of 205 (6%) died or had VT during follow-up; of these, 10 (83%) were in the LGE+ group. In the LGE+ group (1) the rate of death/VT per year was >20× higher than LGE- ( versus %, P<); (2) death/VT were associated with a greater burden of LGE (14±11 versus 5±5%, P<) and right ventricular dysfunction (right ventricular EF 45±12 versus 53±28%, P=). LGE burden was the best predictor of death/VT (area under the receiver-operating characteristics curve, ); for every 1% increase of LGE burden, the hazard of death/VT increased by 8%.

A study done at the School of Biomedical Sciences in Australia examined rats that were fed a high fat and high carbohydrate diet for 16 weeks. The rats that were not treated  developed signs of elevated abdominal and hepatic fat deposition, collagen deposition in heart and liver, cardiac stiffness and oxidative stress markers. The rats that were treated with olive leaf extracts had improved or normalized cardiovascular, hepatic (liver function) and metabolic signs . This study suggests that olive leaf extracts reverse cardiovascular stress and chronic, disease-causing inflammation .

Particulate matter has been studied for its short- and long-term exposure effects on cardiovascular disease . Currently, PM is the major focus, in which gradients are used to determine CVD risk. For every 10 μg/m 3 of PM long-term exposure, there was an estimated 8–18% CVD mortality risk. [46] Women had a higher relative risk (RR) () for PM induced coronary artery disease than men () did. [46] Overall, long-term PM exposure increased rate of atherosclerosis and inflammation. In regards to short-term exposure (2 hours), every 25 μg/m 3 of PM resulted in a 48% increase of CVD mortality risk. [47] In addition, after only 5 days of exposure, a rise in systolic ( mmHg) and diastolic ( mmHg) blood pressure occurred for every μg/m 3 of PM . [47] Other research has implicated PM in irregular heart rhythm, reduced heart rate variability (decreased vagal tone), and most notably heart failure. [47] [48] PM is also linked to carotid artery thickening and increased risk of acute myocardial infarction. [47] [48]

Cannabidiol (CBD) has beneficial effects in disorders as wide ranging as diabetes, Huntington's disease, cancer and colitis. Accumulating evidence now also suggests that CBD is beneficial in the cardiovascular system. CBD has direct actions on isolated arteries, causing both acute and time-dependent vasorelaxation. In vitro incubation with CBD enhances the vasorelaxant responses in animal models of impaired endothelium-dependent vasorelaxation. CBD protects against the vascular damage caused by a high glucose environment, inflammation or the induction of type 2 diabetes in animal models and reduces the vascular hyperpermeability associated with such environments. A common theme throughout these studies is the anti-inflammatory and anti-oxidant effect of CBD. In the heart, in vivo CBD treatment protects against ischaemia-reperfusion damage and against cardiomyopathy associated with diabetes. Similarly, in a different model of ischaemia-reperfusion, CBD has been shown to reduce infarct size and increase blood flow in animal models of stroke, sensitive to 5HT(1A) receptor antagonism. Although acute or chronic CBD treatment seems to have little effect on haemodynamics, CBD reduces the cardiovascular response to models of stress, applied either systemically or intracranially, inhibited by a 5HT(1A) receptor antagonist. In blood, CBD influences the survival and death of white blood cells, white blood cell migration and platelet aggregation. Taken together, these preclinical data appear to support a positive role for CBD treatment in the heart, and in peripheral and cerebral vasculature. However, further work is required to strengthen this hypothesis, establish mechanisms of action and whether similar responses to CBD would be observed in humans.

Cardiovascular damage from steroids

cardiovascular damage from steroids

Cannabidiol (CBD) has beneficial effects in disorders as wide ranging as diabetes, Huntington's disease, cancer and colitis. Accumulating evidence now also suggests that CBD is beneficial in the cardiovascular system. CBD has direct actions on isolated arteries, causing both acute and time-dependent vasorelaxation. In vitro incubation with CBD enhances the vasorelaxant responses in animal models of impaired endothelium-dependent vasorelaxation. CBD protects against the vascular damage caused by a high glucose environment, inflammation or the induction of type 2 diabetes in animal models and reduces the vascular hyperpermeability associated with such environments. A common theme throughout these studies is the anti-inflammatory and anti-oxidant effect of CBD. In the heart, in vivo CBD treatment protects against ischaemia-reperfusion damage and against cardiomyopathy associated with diabetes. Similarly, in a different model of ischaemia-reperfusion, CBD has been shown to reduce infarct size and increase blood flow in animal models of stroke, sensitive to 5HT(1A) receptor antagonism. Although acute or chronic CBD treatment seems to have little effect on haemodynamics, CBD reduces the cardiovascular response to models of stress, applied either systemically or intracranially, inhibited by a 5HT(1A) receptor antagonist. In blood, CBD influences the survival and death of white blood cells, white blood cell migration and platelet aggregation. Taken together, these preclinical data appear to support a positive role for CBD treatment in the heart, and in peripheral and cerebral vasculature. However, further work is required to strengthen this hypothesis, establish mechanisms of action and whether similar responses to CBD would be observed in humans.

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