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Paper text:
the risk of cardiovascular disease and cardiovascular mortality is increased in patients with inflammatory rheumatic diseases compared to the general population or to persons without these diseases .
although an increased risk is most well established for patients with systemic lupus erythematosus and rheumatoid arthritis , some evidence suggests an increased risk also exists for patients with ankylosing spondylitis , psoriasis , and psoriatic arthritis [ 1 - 5 ] .
although the reasons for this increased risk are not completely understood , the association between markers of inflammation , in particular , high - sensitivity c - reactive protein ( hs - crp ) , and cardiovascular risk in patients without known inflammatory disease has led to speculation that systemic inflammation itself may be etiologic [ 6 - 9 ] . evidence that cardiovascular events are reduced in patients who respond to anti - inflammatory treatment supports this view .
the jupiter study ( justification for the use of statins in prevention : an intervention trial evaluating rosuvastatin ) tested whether treatment with rosuvastatin altered the risk of incident cardiovascular events compared to placebo in persons with a normal level of low - density lipoprotein ( ldl ) cholesterol ( less than 130 mg / ml ) but an elevated level of hs - crp ( 2.0 mg / l or higher ) .
persons with systemic inflammatory diseases , including severe arthritis and systemic lupus erythematosus , were excluded , as were those being treated with prednisone and other immunosuppressive medications .
subjects ( n = 17,802 ) were randomized to receive either 20 mg rosuvastatin daily or placebo , for a planned duration of 5 years .
the study 's primary endpoint was the occurrence of a first major cardiovascular event , including myocardial infarction , stroke , hospitalization for unstable angina or arterial revascularization , or death from a cardiovascular cause .
the study was stopped prematurely when an interim analysis found that cardiovascular events were significantly less frequent in the group receiving rosuvastatin .
the primary endpoint was 44% less likely in the rosuvastatin group than in the placebo group , although the rates of events were low in both groups .
there was also a modest reduction in all - cause mortality in the rosuvastatin group .
at 12 months , the median hs - crp level was 37% lower in the rosuvastatin group compared to placebo , from a baseline level of 2.2 mg / l , and median ldl cholesterol was 50% lower in the rosuvastatin group compared to placebo , from a baseline level of 186 mg / dl .
these results indicate that treatment with rosuvastatin can decrease cardiovascular events among patients with an elevated hs - crp level who do not have cholesterol levels elevated to the threshold customarily used to begin treatment
. one possible implication of these results is that primary prevention strategies should be broadened to treat with statins those whose only cardiac risk factor is an elevated hs - crp level . but is this an appropriate conclusion ?
although subjects were selected based on both an elevated hs - crp level and a normal ldl cholesterol level , the trial did not include a group with low hs - crp levels and , therefore , did not isolate the benefit to patients with elevated hs - crp levels specifically . nor
did it test hs - crp as a screening tool to target treatment , which would have required a parallel arm of subjects who had not been tested for hs - crp and were treated without regard to hs - crp level . in the strictest interpretation , the jupiter trial expands the potential mechanisms by which statins reduce cardiovascular events to include reductions in hs - crp levels . whether this effect is completely independent of the hypocholersterolemic effect is uncertain .
given the elevated cardiovascular risk experienced by patients with inflammatory rheumatic diseases , and the association of elevated crp levels with cardiovascular disease , how should the results of the jupiter trial be applied to patients with inflammatory rheumatic diseases ?
if hs - crp levels in persons without inflammatory diseases reflect inflammation in atherosclerotic endothelial lesions , while hs - crp ( or crp ) levels in patients with inflammatory diseases primarily reflect inflammation outside the atherosclerotic endothelial lesions , elevated hs - crp levels would not be specific to the etiologic target in patients with inflammatory diseases . in this case , targeting treatment based on hs - crp would not be helpful , and treatment might not be expected to have the same effects .
statins have multiple immunomodulatory actions , which may have a role in their cardioprotective effects .
differences in activation or regulation of these immune and inflammatory pathways between patients with chronic inflammatory rheumatic diseases and people without these diseases complicate using the findings in non - rheumatic cohorts to predict effects in rheumatic disease cohorts . also to be considered
is whether any benefit of statins for primary prevention would be attenuated or negated by anti - rheumatic treatments , particularly chronic corticosteroids .
lastly , the long - term safety of statins and unknown risks of prolonged marked hypocholesterolemia would need to be balanced against the potential benefits . given the difficulty applying the results of the jupiter trial to patients with inflammatory diseases
, it would be premature to recommend statins for primary prevention of cardiovascular events in patients with inflammatory rheumatic diseases .
rather , cardiac risk factor assessment and modification should be enforced , while awaiting the results of ongoing or recently completed studies specifically investigating statins for primary cardiovascular disease prevention in systemic lupus erythematosus and rheumatoid arthritis [ 13 - 15 ] .
patients with inflammatory rheumatic diseases have an increased risk of cardiovascular disease , raising questions of whether primary prevention strategies that are more aggressive than cardiac risk factor modification alone should be implemented . 
 recent trials demonstrating the efficacy of statins in reducing rates of cardiovascular events in healthy persons with elevated levels of c - reactive protein broaden the potential protective mechanisms of statins , but do not directly translate to primary cardiovascular disease prevention in patients with inflammatory rheumatic diseases .