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Coronary heart disease in lupus – are traditional risk factors solely to blame?

February 28, 2012

The increased risk of atherosclerotic coronary heart disease (CHD) in systemic lupus erythematosus (SLE) is now widely recognised. The magnitude of risk relative to the general population is greatest for young women aged in their thirties and forties, who are at 50 times increased risk of having myocardial infarction (MI) compared to age and sex-matched peers. In SLE, the overall lifetime risk of having a coronary ‘event’ such as angina or MI is approximately 10-11%, making CHD a major cause of mortality in this disease. Patients with SLE also have an increased risk of ischemic stroke and peripheral vascular disease; this too is largely due to atherosclerosis. Studies have shown that the fatality rate for ‘first’ coronary events in SLE is even greater than with diabetes. Further, patients with SLE are more likely to have prolonged hospitalisation for MI compared with those who have diabetes. Inflammation is thought to be the pivotal link between SLE and atherosclerotic vascular disease, with immune mechanisms thought to play a key role in plaque formation and rupture.

...

Role of disease activity – measures of disease activity in SLE such as the SLE disease activity index, have been repeatedly shown to have a positive association with CHD risk. This means that those with the greatest cumulative burden of disease activity are those at highest risk for CHD. This is not surprising as inflammation is considered the key link between atherosclerosis and SLE. This association underscores the importance of adequate treatment of active disease in SLE. Up to 50% of patients with SLE live in a state of persistent disease activity, even in a specialised care setting. However, the potential benefit of immunosuppressive therapy needs to be balanced against potential toxicity, particularly the increased risk of infection. Clearly there remains a need for more effective and less toxic therapies in SLE, not only to control disease activity acutely, but also to prevent sequelae such as CHD.

Corticosteroids: friend or foe? At present, corticosteroids are the cornerstone of treatment of SLE flares. Corticosteroid side effects include hypertension, hyperlipidemia, abdominal obesity and diabetes. Whilst in many studies corticosteroid use is associated with increased CHD risk in SLE, agents such as prednisone may also have an indirect protective effect through control of disease activity. Optimising corticosteroid dose and duration of therapy in SLE remains a challenge.

Hydroxychloroquine – There is emerging evidence regarding the protean beneficial effects of hydroxychloroquine in SLE, including control of mild disease activity, prevention of flares, and reduction of CHD-related mortality. Possible mechanisms for the cardioprotective effect of hydroxychloroquine include reduction in lipid levels and blood glucose. At present, hydroxychloroquine is recommended as staple therapy in all patients with SLE, including during pregnancy.

Markers of inflammation – The role of inflammation in atherosclerosis, even in the general population, is becoming increasingly apparent. In large population studies, high-sensitivity C-reactive protein, a non-specific marker of inflammation has been shown to predict CHD events, independently of traditional risk factors. In SLE, hsCRP levels fluctuate greatly over time due to the relapsing remitting nature of the disease, and its therapies. However, despite this variability over time, mean hsCRP level appears to be predictive of CHD events in SLE, even after adjusting for the Framingham risk score and cumulative disease activity score.

...

Obesity and physical inactivity – In the general population, metabolic syndrome, a constellation of abdominal obesity, hypertension and insulin resistance, confers an increased risk of CHD that is greater than the sum of its parts, indicating a degree of synergy among certain cardiovascular risk factors. Metabolic syndrome is common in SLE, affecting 18% of patients, and is a cardiovascular risk factor that is potentially modifiable through weight reduction and increased physical exercise.

Smoking – Analysis of data from large lupus cohorts has revealed that up to 20% of patients with SLE are smokers.

...

Prevention of CHD in SLE – There is surprisingly little direct evidence available to support the use of various preventive strategies such as treatment of hypertension and hyperlipidemia, and change in lifestyle, in modifying risk of CHD in SLE. In one study, atorvastatin did not reduce subclinical measures of atherosclerosis over 2 years in patients with SLE. In the Toronto lupus cohort wherein patients are treated with statins at physician discretion, a mean LDL-C less than 2.0 mmol/L over time, has a negative predictive value for CHD events of 91% (95% CI: 70% to 99%). This is indirect evidence that reduction of LDL-C to levels as low as 2.0 mmol/L has the potential to dramatically reduce CHD risk in SLE.  Whilst the role of lipid lowering therapy in reducing CHD risk in SLE may only be conclusively evaluated in a randomised controlled trial, feasibility and ethical considerations pose major challenges in this regard.

Read the full article here

Source erheumatology.tv


Coronary heart disease in lupus – are traditional risk factors solely to blame?

February 28, 2012

The increased risk of atherosclerotic coronary heart disease (CHD) in systemic lupus erythematosus (SLE) is now widely recognised. The magnitude of risk relative to the general population is greatest for young women aged in their thirties and forties, who are at 50 times increased risk of having myocardial infarction (MI) compared to age and sex-matched peers. In SLE, the overall lifetime risk of having a coronary ‘event’ such as angina or MI is approximately 10-11%, making CHD a major cause of mortality in this disease. Patients with SLE also have an increased risk of ischemic stroke and peripheral vascular disease; this too is largely due to atherosclerosis. Studies have shown that the fatality rate for ‘first’ coronary events in SLE is even greater than with diabetes. Further, patients with SLE are more likely to have prolonged hospitalisation for MI compared with those who have diabetes. Inflammation is thought to be the pivotal link between SLE and atherosclerotic vascular disease, with immune mechanisms thought to play a key role in plaque formation and rupture.

...

Role of disease activity – measures of disease activity in SLE such as the SLE disease activity index, have been repeatedly shown to have a positive association with CHD risk. This means that those with the greatest cumulative burden of disease activity are those at highest risk for CHD. This is not surprising as inflammation is considered the key link between atherosclerosis and SLE. This association underscores the importance of adequate treatment of active disease in SLE. Up to 50% of patients with SLE live in a state of persistent disease activity, even in a specialised care setting. However, the potential benefit of immunosuppressive therapy needs to be balanced against potential toxicity, particularly the increased risk of infection. Clearly there remains a need for more effective and less toxic therapies in SLE, not only to control disease activity acutely, but also to prevent sequelae such as CHD.

Corticosteroids: friend or foe? At present, corticosteroids are the cornerstone of treatment of SLE flares. Corticosteroid side effects include hypertension, hyperlipidemia, abdominal obesity and diabetes. Whilst in many studies corticosteroid use is associated with increased CHD risk in SLE, agents such as prednisone may also have an indirect protective effect through control of disease activity. Optimising corticosteroid dose and duration of therapy in SLE remains a challenge.

Hydroxychloroquine – There is emerging evidence regarding the protean beneficial effects of hydroxychloroquine in SLE, including control of mild disease activity, prevention of flares, and reduction of CHD-related mortality. Possible mechanisms for the cardioprotective effect of hydroxychloroquine include reduction in lipid levels and blood glucose. At present, hydroxychloroquine is recommended as staple therapy in all patients with SLE, including during pregnancy.

Markers of inflammation – The role of inflammation in atherosclerosis, even in the general population, is becoming increasingly apparent. In large population studies, high-sensitivity C-reactive protein, a non-specific marker of inflammation has been shown to predict CHD events, independently of traditional risk factors. In SLE, hsCRP levels fluctuate greatly over time due to the relapsing remitting nature of the disease, and its therapies. However, despite this variability over time, mean hsCRP level appears to be predictive of CHD events in SLE, even after adjusting for the Framingham risk score and cumulative disease activity score.

...

Obesity and physical inactivity – In the general population, metabolic syndrome, a constellation of abdominal obesity, hypertension and insulin resistance, confers an increased risk of CHD that is greater than the sum of its parts, indicating a degree of synergy among certain cardiovascular risk factors. Metabolic syndrome is common in SLE, affecting 18% of patients, and is a cardiovascular risk factor that is potentially modifiable through weight reduction and increased physical exercise.

Smoking – Analysis of data from large lupus cohorts has revealed that up to 20% of patients with SLE are smokers.

...

Prevention of CHD in SLE – There is surprisingly little direct evidence available to support the use of various preventive strategies such as treatment of hypertension and hyperlipidemia, and change in lifestyle, in modifying risk of CHD in SLE. In one study, atorvastatin did not reduce subclinical measures of atherosclerosis over 2 years in patients with SLE. In the Toronto lupus cohort wherein patients are treated with statins at physician discretion, a mean LDL-C less than 2.0 mmol/L over time, has a negative predictive value for CHD events of 91% (95% CI: 70% to 99%). This is indirect evidence that reduction of LDL-C to levels as low as 2.0 mmol/L has the potential to dramatically reduce CHD risk in SLE.  Whilst the role of lipid lowering therapy in reducing CHD risk in SLE may only be conclusively evaluated in a randomised controlled trial, feasibility and ethical considerations pose major challenges in this regard.

Read the full article here

Source erheumatology.tv



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