This hypothesis has recently been tested in seven studies summarized in Table 1. Main studies addressing the risk of arterial cardiovascular events in patients with VTE. The incidence of arterial cardiovascular events after VTE was assessed for the first time in a long-term prospective study on the long-term follow-up in patients with a first episode of pulmonary embolism PE , of whom with idiopathic PE and with PE associated with transient risk factors.
After a median follow-up of 38 months, a cardiovascular event occurred in 47 patients with idiopathic PE 7. Twenty patients with idiopathic PE 3. After adjusting for age, the idiopathic nature of the index PE was confirmed to be an independent risk factor for arterial cardiovascular events at the long-term follow-up.
Later, we reported the results of a prospective follow-up study in consecutive patients with a first VTE episode. After a median follow-up of 48 and 51 months, respectively, at least one symptomatic atherosclerotic complication was detected in of the patients After adjusting for age and other risk factors of atherosclerosis, the HR for symptomatic atherosclerotic complications in patients with VTE of unknown origin compared to those with secondary VTE was 1.
When the analysis was restricted to patients without previous symptomatic atherosclerosis, the HR became 1. In the recently published study by Schulman and colleagues, reporting on the extended year follow-up of the DURAC study in patients with VTE who had been randomized to receive six weeks or six months of vitamin K antagonists, 27 the overall mortality Bova and colleagues explored the rate of subsequent arterial events in patients with unprovoked VTE and control subjects.
They collected information about cardiovascular risk factors hypertension, hypercholesterolemia, diabetes, obesity, and smoke at the time of VTE episode, or corresponding date for the controls, and considered the follow-up from this time. During a mean follow-up of 43 months there were 16 arterial events in the VTE patients and six in the control group, corresponding to an HR of 2.
The difference remained significant after adjusting for age and other cardiovascular risk factors adjusted HR, 2. Overall mortality was also higher in the VTE patients 12 vs 4 deaths.
Young and colleagues followed over five years a cohort of patients with acute DVT. As expected, patients with residual thrombus on follow-up ultrasound were at higher risk of recurrence, which remained significant after multivariate adjustment for age, gender and malignancy adjusted HR, 2.
The risk of death was increased in patients with residual thrombus at follow-up scan, and this risk persisted after multivariate analysis of age, gender and malignancy adjusted RR, 2. There was a trend towards increased vascular death in the patients with residual thrombus on follow up ultrasound scan, which did not reach significance HR, 4.
The increased risk of death in patients with residual thrombus, with a trend towards increased vascular death, may suggest that failure of thrombus resolution, a well known risk factor of recurrent thromboembolism, 31 is a marker of more global vascular dysfunction. In a recent population-based cohort study using nationwide Danish medical databases, Sorensen and colleagues assessed the risk of hospitalization due to myocardial infarction, stroke and transient ischemic attack among 25, patients with DVT, 16, patients with PE, and , population controls.
For patients with DVT, the relative risks varied from 1. For patients with PE, the relative risks were 2. Spencer and colleagues performed a longitudinal matched cohort study utilizing multiple administrative databases.
Patients 20—39 years of age presenting with unprovoked VTE had an increased risk of myocardial infarction HR, 3. There was no significant relationship between unprovoked VTE and AMI among patients 40—64 years old, with or without atherosclerotic risk factors. All together, the results of these studies are in keeping with the observation of a higher prevalence of carotid atherosclerosis in patients with unprovoked DVT than in matched control individuals, 7 and suggest that patients with VTE have also an increased risk of subsequent symptomatic arterial cardiovascular events.
This implies that arterial and venous thrombosis may share common mechanisms or risk factors, and may have a common origin in abnormalities of various blood constituents. We speculate that venous and arterial thrombosis are two aspects of the same disease ie, thrombosis , and that this disease may electively affect genetically predisposed individuals resulting in clinically manifestations that are, in turn, depending on a variety of elements including the age of patients, their lifestyle, and the occurrence of co-morbidities and circumstantial factors: the venous thrombotic events being more frequent, for example, after triggering risk factors such as surgery or trauma, and the arterial thrombotic events being more frequent in subjects who have developed atherosclerosis.
These findings have several implications for both research and medical practice. Patients with VTE of unknown origin could be examined for asymptomatic atherosclerosis, in order to modify aggressively the risk profile in those with abnormal test results.
Measures could include appropriate counseling about lifestyle changes and control of risk factors for atherosclerosis. Interestingly enough, lifestyle factors are likely to have a major impact on the risk of VTE. A diet including more plant food and fish and less red and processed meat, 34 the supplementation of vitamin E, 35 regular sports activities, 36 and alcohol consumption 37 have recently been found to be associated with a lower incidence of venous thrombosis.
Consistent with these findings are the results of a prospective cohort study conducted in Sweden on 40, Swedish women who were followed-up for a mean of 11 years: female nonsmokers who were physically active and who consumed alcohol in moderation were found to have a lower risk of VTE. In addition, a potential role for prophylaxis of both recurrent VTE and arterial cardiovascular events with antiplatelet therapy or statins may be explored.
Interest in statins has increased, given recent data that suggest a potential role both in controlling the development of atherosclerotic lesions and in lowering the risk of venous thromboembolism.
The currently available evidence for a role of aspirin in VTE prevention and treatment is quite limited. In conclusion, the separate nature of arterial and venous thrombotic disorders has been challenged.
National Center for Biotechnology Information , U. Journal List Clin Epidemiol v. Clin Epidemiol. Published online Aug 9. Paolo Prandoni. Author information Copyright and License information Disclaimer. This is an Open Access article which permits unrestricted noncommercial use, provided the original work is properly cited. This article has been cited by other articles in PMC. Abstract An increasing body of evidence suggests the likelihood of a link between venous and arterial thrombosis.
Keywords: venous thromboembolism, deep vein thrombosis, pulmonary embolism, myocardial infarction, ischemic stroke, atherosclerosis. Introduction Venous and arterial thrombotic disorders have long been viewed as separate pathophysiological entities, partly as a result of the obvious anatomical differences, as well as their distinct clinical presentations. You have successfully created a MyAccess Profile for alertsuccessName.
Previous Chapter. Next Chapter. Freedman J. Arterial and Venous Thrombosis. Dennis Kasper, et al. Harrison's Principles of Internal Medicine, 19e. McGraw Hill; Accessed November 12, Arterial and venous thrombosis. McGraw Hill.
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Please Wait. Arterial thrombosis is often associated with atherosclerosis. Atherosclerosis is the development of plaques, or fatty hardenings, on the inner wall of an artery. Plaques cause the artery to narrow. This increases the amount of pressure in the blood vessel. If this pressure becomes intense enough, the plaque can become unstable and rupture.
Sometimes when a plaque ruptures the immune system overreacts. This can lead to the development of a large clot and a life-threatening condition, like a heart attack or stroke. When a blood vessel wall is injured, blood cells, called platelets and proteins, form a solid mass over the wound. This mass is called a thrombus, or blood clot.
The clot helps seal off the injury site to limit bleeding and protect it during healing. This is similar to a scab on an external wound. Once the wound has healed, blood clots typically dissolve on their own.
This can lead to serious health risks by reducing blood flow and causing damage or death to the involved tissue that it supplies. Embolisms can also occur when other substances are trapped in blood vessels, like air bubbles, fat molecules, or bits of plaque. There is no specific test used to diagnose thrombosis and embolism, although duplex ultrasound, or the use of sound waves to create images of flowing blood, is commonly used.
Other tests that may be used to help diagnose or assess abnormal blood clots or obstructions include:. In most cases, medical treatment depends on the type, extent, and location of the blood clot or obstruction. Certain lifestyle changes or preventative medications can help treat clots or reduce your risk of developing them.
Embolism is often considered more dangerous than mild to moderate thrombosis because embolism tends to obstruct the entire blood vessel. For mild cases of thrombosis and embolism, symptoms may resolve within a few days to weeks of medication and lifestyle changes. The outlook for more severe cases depends mostly on the type, extent, and location of the clot or obstruction.
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