M-MODE AND DOPPLER-ECHOCARDIOGRAPHIC ASSESSMENT OF LEFT-VENTRICULAR DIASTOLIC FUNCTION IN PRIMARY ANTIPHOSPHOLIPID SYNDROME

Background-High titres of serum antiphospholipid antibodies are a poss ible pathogenic factor for cardiac lesions in patients with systemic l upus erythematosus. Objective-To test the hypothesis of a causal link between high titres of antiphospholipid antibodies in the serum and my ocardial involvement in patients without systemic lupus erythematosus. Patients and design-18 patients with primary antiphospholipid syndrom e (recurrent fetal loss, arterial and/or venous thrombosis, high titre s of antiphospholipid antibodies, and no criteria for systemic lupus e rythematosus) were prospectively studied by cross sectional, M mode, a nd pulsed Doppler echocardiography, and compared with 18 healthy contr ols. 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. Fou r computerised M mode indices were also measured: peak rate of left ve ntricular enlargement in diastole, peak rate of posterior wall thinnin g, 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 an d lower values for early to late mitral peak outflow velocity ratio, r ate of deceleration of early mitral outflow, peak rate of left ventric ular enlargement in diastole, peak rate of posterior wall thinning, pe ak velocity of lengthening of the posterior wall and velocity of circu mferential chamber lengthening. Conclusion-This abnormal pattern refle cts 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 sugg est that high serum titres of antiphospholipid antibodies may be assoc iated with subclinical myocardial damage.