News about Health (Part 10)

Thrombin, Inflammation, and Cardiovascular Disease: Atherothrombosis

Thrombin, Inflammation, and Cardiovascular Disease: AtherothrombosisWhile it remains unproven whether any of these mechanisms are actually at play in situ, given all the available data it seems likely that higher fibrinogen may well not only reflect the low-grade inflammation caused by the atherothrombosis, but also participate in that process, allowing it to proceed at a faster rate. This “positive feedback” is illustrated in Figure 1.

Thrombin, Inflammation, and Cardiovascular Disease: CVD risk

To support this position, studies of the plasma levels of prothrombin (a key procoagulant protein, but not an inflammation-sensitive protein) and/or the prothrombin G20210A genotype associated with plasma levels, generally have been null for CVD risk in most cases while consistently positive for venous thrombosis. Also, several studies have examined the anticoagulant proteins and their relationship to CVD. As an ancillary study to the Thrombolysis in Myocardial Infarction Phase II trial of thrombolytic therapy, we demonstrated that in those entering the health system with MIs, anticoagulant proteins, such as protein C and antithrombin, were elevated, not decreased. We have also demonstrated that in otherwise healthy adults tissue factor pathway inhibitor levels were higher, not lower, in those with increased measures of subclinical disease based on ankle-brachial BP index and carotid ultrasonography.

Thrombin, Inflammation, and Cardiovascular Disease: Atherosclerosis, Thrombosis, and Inflammation

Thrombin, Inflammation, and Cardiovascular Disease: Atherosclerosis, Thrombosis, and InflammationThere Is a Complex Interplay Among Atherosclerosis, Thrombosis, and Inflammation
Atherosclerotic coronary heart disease commonly manifests itself clinically via a thrombotic event: so-called “atherothrombosis,” especially in younger men. As mentioned above, this has been clearly understood only since the early 1970s. As an overview, the process of blood clotting is comprised of coagulation, limited and controlled by anticoagulation; and the counterbalancing process of fibrinolysis, limited and controlled by antifibrinolysis. more

Thrombin, Inflammation, and Cardiovascular Disease: Thrombotic disease

Overall, a meta-analysis demonstrated moderate risk prediction for d-dimer. The most likely interpretation of these data are that the degree of atherosclerosis and vascular damage causes changes in coagulation status, not vice versa; ie, it does not appear that a preexisting hypercoag-ulable state is in the causal pathway of atherosclerotic disease and CVD events. This position is supported by the findings such as those of Lowe et al, in which future ischemic events were predicted by d-dimer levels but not by other markers of procoagulant activity, such as prothrombin fragment F1 + 2 and thrombin-antithrombin complex (measures of thrombin generation), or by factor VII coagulant activity (factor VIIc, which at least partly reflects factor VII activation). Link

Thrombin, Inflammation, and Cardiovascular Disease: MI and CVD death

Thrombin, Inflammation, and Cardiovascular Disease: MI and CVD deathIs There a Hypercoagulable State That Predisposes to CVD?
Meade and colleagues at the Northwick Park Heart Study produced pioneering research into the molecular epidemiology of coagulation and fibrinolysis, which suggested that a preexisting hypercoagulable state might be present in those most at risk for MI and CVD death. While the research that followed their work has provided little support for this as a general condition—for example, it does not appear that elevations in factor VIIc levels are a major risk factor, as they originally proposed—their results for fibrinogen and factor VIIIc have held up in many other studies. We now interpret these results for fibrinogen and factor VIII as probably best supportive of inflammation rather than hypercoagulability.

Thrombin, Inflammation, and Cardiovascular Disease: Thrombin-activated fibrinolysis inhibitor

Thrombin is also responsible for the activation of a newly discovered major thrombosis regulator, thrombin-activated fibrinolysis inhibitor, also discussed in more detail by Dr. Nesheim elsewhere in this supplement. Thrombin-activated fibrinolysis inhibitor appears to play a major role in down-regulating fibrinolysis, which may have important implications in heart disease, as has been proposed.

Thrombin, Inflammation, and Cardiovascular Disease: Thrombin

Thrombin, Inflammation, and Cardiovascular Disease: ThrombinThe precipitating cause is less apparent in these cases, and one may speculate that transient platelet aggregation at the site of lesion fracture or erosion, which may be tolerated if occurring in younger hearts, may prove fatal in older, weaker hearts. The atherosclerotic burden associated with events later in life is much greater than that associated with events in younger people, where the actual plaque burden may be limited. comments

Thrombin, Inflammation, and Cardiovascular Disease: Clinical CVD

A major form of CVD is myocardial infarction (MI); in the early 1970s, it became evident, through the work of DeWood and colleagues” and others, that the proximal event in MI is commonly an occlusive blood clot in a coronary artery. The term vulnerable plaque has been used to describe a form of atherosclerosis characterized by rapid, focal lipid accumulation, with the development of a large pool of subendothelial fat covered by a thin, mechanically fragile cap.

Thrombin, Inflammation, and Cardiovascular Disease

Thrombin, Inflammation, and Cardiovascular DiseaseAtherosclerosis and resulting clinical cardiovascular disease (CVD) are complex pathophysiologic processes involving a large number of genes and gene products in complicated interactions with a variety of environmental influences. An enormous body of research over the last 20 years has helped us understand that many of the biochemical processes involved in CVD are the same as those involved in ongoing defense against a hostile world, including blood coagulation, inflammation, and immune response.

Comparison of Function of Commercially Available Pleural Drainage Units and Catheters: Conclusion

All other PDU models demonstrated significant pressure accuracy error differences between the two external suction settings (manufacturer-suggested wall suction setting vs full wall suction) in the negative direction (delivering more negative pressure than the PDU test value). The least accurate PDU at full wall suction was the Thora-Seal III, with a mean error of 27%. This translates to a mean delivered negative water pressure of 25.4 cm H2O.

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