Coronary Flow May Predict Early Heart Disease in SLE

New evidence suggests premenopausal women with systemic lupus erythematosus also have impaired coronary microvascular function, supporting “the notion that many of these young patients have subclinical coronary artery disease,” wrote Dr. Kumiko Hirata from Columbia University, New York, and colleagues.

“Systemic lupus erythematosus (SLE) patients have a significantly increased risk of coronary heart disease that is not fully explained by the classic risk factors,” the study's investigators wrote.

“Measurements of coronary vasomotor function may therefore provide more relevant information with which to predict and assess potential cardiovascular damage related to limited vascular responsiveness,” they added.

Because invasive measurements of coronary flow are hard to justify in young patients, the investigators used noninvasive transthoracic Doppler echocardiography (TTDE) to estimate coronary flow velocity reserve (CFVR).

The study looked at 38 premenopausal women, (27 Chinese, 11 American Hispanic) 19 of whom had SLE, and 19 controls. All were assessed following an overnight fast.

In order to avoid confounders that might influence endothelial function, exclusion criteria included a history of smoking, diabetes mellitus, hypercholesterolemia, and cardiovascular disease (Arthritis Rheum. 2007;56:1904-9).

Using TTDE, the investigators recorded the left anterior descending coronary artery flow under both basal and hyperemic conditions in all 38 study participants.

The researchers measured serum levels of lipids, high-sensitivity C-reactive protein (hsCRP), and serum anticardiolipin antibodies, and assessed disease activity with the SLE Disease Activity Index (SLEDAI).

The CFVR in SLE patients was found to be significantly lower than that of controls, after adjustment for body mass index and serum triglyceride levels (the latter being nonsignificantly higher in SLE patients, compared with the control group), reported the authors.

“The CFVR was not significantly correlated with the SLEDAI score, disease duration, level of anticardiolipin antibody, hsCRP, total cholesterol, LDL cholesterol, triglycerides, or HDL cholesterol, ethnicity, or type of immunosuppressive drug used,” they added.

Moreover, the significance of a blunted CFVR in SLE “may reflect functional alterations in the endothelium, vascular smooth muscle cells, or both.” They added that because the TTDE measurement of CFVR is relatively new, further study is needed.

“Altered microvascular function may provide a study model of factors that contribute to coronary artery disease in SLE. It may help us to define the interplay between autoimmunity and atherogenesis and help us to better understand the pathophysiologic process of atherogenesis in general,” the researchers concluded.

New evidence suggests premenopausal women with systemic lupus erythematosus also have impaired coronary microvascular function, supporting “the notion that many of these young patients have subclinical coronary artery disease,” wrote Dr. Kumiko Hirata from Columbia University, New York, and colleagues.

“Systemic lupus erythematosus (SLE) patients have a significantly increased risk of coronary heart disease that is not fully explained by the classic risk factors,” the study's investigators wrote.

“Measurements of coronary vasomotor function may therefore provide more relevant information with which to predict and assess potential cardiovascular damage related to limited vascular responsiveness,” they added.

Because invasive measurements of coronary flow are hard to justify in young patients, the investigators used noninvasive transthoracic Doppler echocardiography (TTDE) to estimate coronary flow velocity reserve (CFVR).

The study looked at 38 premenopausal women, (27 Chinese, 11 American Hispanic) 19 of whom had SLE, and 19 controls. All were assessed following an overnight fast.

In order to avoid confounders that might influence endothelial function, exclusion criteria included a history of smoking, diabetes mellitus, hypercholesterolemia, and cardiovascular disease (Arthritis Rheum. 2007;56:1904-9).

Using TTDE, the investigators recorded the left anterior descending coronary artery flow under both basal and hyperemic conditions in all 38 study participants.

The researchers measured serum levels of lipids, high-sensitivity C-reactive protein (hsCRP), and serum anticardiolipin antibodies, and assessed disease activity with the SLE Disease Activity Index (SLEDAI).

The CFVR in SLE patients was found to be significantly lower than that of controls, after adjustment for body mass index and serum triglyceride levels (the latter being nonsignificantly higher in SLE patients, compared with the control group), reported the authors.

“The CFVR was not significantly correlated with the SLEDAI score, disease duration, level of anticardiolipin antibody, hsCRP, total cholesterol, LDL cholesterol, triglycerides, or HDL cholesterol, ethnicity, or type of immunosuppressive drug used,” they added.

Moreover, the significance of a blunted CFVR in SLE “may reflect functional alterations in the endothelium, vascular smooth muscle cells, or both.” They added that because the TTDE measurement of CFVR is relatively new, further study is needed.

“Altered microvascular function may provide a study model of factors that contribute to coronary artery disease in SLE. It may help us to define the interplay between autoimmunity and atherogenesis and help us to better understand the pathophysiologic process of atherogenesis in general,” the researchers concluded.

New evidence suggests premenopausal women with systemic lupus erythematosus also have impaired coronary microvascular function, supporting “the notion that many of these young patients have subclinical coronary artery disease,” wrote Dr. Kumiko Hirata from Columbia University, New York, and colleagues.

“Systemic lupus erythematosus (SLE) patients have a significantly increased risk of coronary heart disease that is not fully explained by the classic risk factors,” the study's investigators wrote.

“Measurements of coronary vasomotor function may therefore provide more relevant information with which to predict and assess potential cardiovascular damage related to limited vascular responsiveness,” they added.

Because invasive measurements of coronary flow are hard to justify in young patients, the investigators used noninvasive transthoracic Doppler echocardiography (TTDE) to estimate coronary flow velocity reserve (CFVR).

The study looked at 38 premenopausal women, (27 Chinese, 11 American Hispanic) 19 of whom had SLE, and 19 controls. All were assessed following an overnight fast.

In order to avoid confounders that might influence endothelial function, exclusion criteria included a history of smoking, diabetes mellitus, hypercholesterolemia, and cardiovascular disease (Arthritis Rheum. 2007;56:1904-9).

Using TTDE, the investigators recorded the left anterior descending coronary artery flow under both basal and hyperemic conditions in all 38 study participants.

The researchers measured serum levels of lipids, high-sensitivity C-reactive protein (hsCRP), and serum anticardiolipin antibodies, and assessed disease activity with the SLE Disease Activity Index (SLEDAI).

The CFVR in SLE patients was found to be significantly lower than that of controls, after adjustment for body mass index and serum triglyceride levels (the latter being nonsignificantly higher in SLE patients, compared with the control group), reported the authors.

“The CFVR was not significantly correlated with the SLEDAI score, disease duration, level of anticardiolipin antibody, hsCRP, total cholesterol, LDL cholesterol, triglycerides, or HDL cholesterol, ethnicity, or type of immunosuppressive drug used,” they added.

Moreover, the significance of a blunted CFVR in SLE “may reflect functional alterations in the endothelium, vascular smooth muscle cells, or both.” They added that because the TTDE measurement of CFVR is relatively new, further study is needed.

“Altered microvascular function may provide a study model of factors that contribute to coronary artery disease in SLE. It may help us to define the interplay between autoimmunity and atherogenesis and help us to better understand the pathophysiologic process of atherogenesis in general,” the researchers concluded.