Key result
Primary antiphospholipid syndrome was associated with impaired left ventricular relaxation and filling dynamics compared to healthy controls, suggesting subclinical myocardial damage.
Why the study?
Is primary antiphospholipid syndrome associated with subclinical impairment of left ventricular diastolic function?
Cross-Sectional (n=36)
Is primary antiphospholipid syndrome associated with subclinical impairment of left ventricular diastolic function?
Primary antiphospholipid syndrome is associated with subclinical impairment of left ventricular diastolic function, suggesting a potential link between high antiphospholipid antibody titers and myocardial damage.
Answers are grounded in this paper and cite their sources.
Subclinical LV diastolic dysfunction occurs in primary APS; leaves open whether antibodies contribute causally or merit screening.
BACKGROUND: High titres of serum antiphospholipid antibodies are a possible pathogenic factor for cardiac lesions in patients with systemic lupus erythematosus. OBJECTIVE: To test the hypothesis of a causal link between high titres of antiphospholipid antibodies in the serum and myocardial involvement in patients without systemic lupus erythematosus. PATIENTS AND DESIGN: 18 patients with primary antiphospholipid syndrome (recurrent fetal loss, arterial and/or venous thrombosis, high titres of antiphospholipid antibodies, and no criteria for systemic lupus erythematosus) were prospectively studied by cross sectional, M mode, and pulsed Doppler echocardiography, and compared with 18 healthy controls. The pulsed Doppler indices of left ventricular diastolic function included isovolumic relaxation time and four mitral outflow indices: peak velocity of early flow, peak velocity of late flow, early to late peak flow velocity ratio, and rate of deceleration of early flow. Four computerised M mode indices were also measured: peak rate of left ventricular enlargement in diastole, peak rate of posterior wall thinning, peak velocity of lengthening of the posterior wall, and velocity of circumferential chamber lengthening. RESULTS: Compared with controls, patients with primary antiphospholipid syndrome had higher values for isovolumic relaxation time and peak velocity of late mitral outflow and lower values for early to late mitral peak outflow velocity ratio, rate of deceleration of early mitral outflow, peak rate of left ventricular enlargement in diastole, peak rate of posterior wall thinning, peak velocity of lengthening of the posterior wall and velocity of circumferential chamber lengthening. CONCLUSION: This abnormal pattern reflects an impairment of myocardial relaxation and filling dynamics of the left ventricle in patients with primary antiphospholipid syndrome who were free of any clinically detectable heart disease. These data suggest that high serum titres of antiphospholipid antibodies may be associated with subclinical myocardial damage.
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Coudray et al. (1995) conducted a cross-sectional in Primary antiphospholipid syndrome (n=36). Primary antiphospholipid syndrome vs. Healthy controls was evaluated on Left ventricular diastolic function indices (isovolumic relaxation time, mitral outflow indices, and M mode indices). Primary antiphospholipid syndrome was associated with impaired left ventricular relaxation and filling dynamics compared to healthy controls, suggesting subclinical myocardial damage.
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