Endomyocardial fibrosis associated with antiphospholipid syndrome

Abstract

Objective-To determine whether simple, readily applicable ECG criteria will allow early prediction of inadequate (< TIMI 3) flow in the infarct related vessel in patients receiving thrombolytic treatment for acute myocardial infarction; and to determine the success of streptokinase in achieving adequate antegrade flow in the infarct related vessel two hours after starting treatment. Design-Cohort study. Setting-Regional cardiothoracic unit. Patients-100 sequential patients with acute myocardial infarction. Interventions-Coronary angiography two hours after the initiation of thrombolytic treatment, proceeding to rescue angioplasty for inadequate flow in the infarct related vessel where appropriate. Main outcome measures-Sensitivity, specificity, positive predictive value, negative predictive value, and accuracy of six ECG criteria for the detection of inadequate antegrade flow in the infarct related vessel. Results-The ECG test that performed best as a positive test for < TIMI 3 flow in the infarct related vessel was < 50% resolution of the ST segment elevation in the worst lead and no accelerated idioventricular rhythm. This had a sensitivity of 81%, specificity of 88%, positive predictive value of 87%, negative predictive value of 83%, and overall accuracy of 85%. Conclusions-Sensitive, specific, and simple ECG criteria are defined for diagnosing failure of thrombolytic treatment with streptokinase. These allow the early detection of patients at high risk of further adverse events from a persistently occluded vessel. They may be used without recourse to sophisticated equipment or complex analyses. Such patients can then be considered for alternative treatments or enrolment into appropriate research protocols. (Heart 2000;84:149-156)

Antiphospholipid syndrome and the heart: A case series and literature review

“…The histological findings range from microvascular thrombosis to endomyocardial fibrosis [74][75][76]. Histological evidence of inflammation, intramyocardial arteriolar immune deposits and widespread thrombosis with surrounding areas of microinfarction, have been reported [87][88][89].…”

“…Ventricular dysfunction in APS may result from the direct effect of the antibodies in the myocardium, or from myocardial ischaemia in form of thrombosis of the coronary arteries or microvascular thrombosis [74][75][76]. Of these, microvascular injury is probably the most feared complication and it may go unrecognized because its detection requires specific diagnostic techniques [15].…”

Trombo biventricular e fibrose endomiocárdica na síndrome antifosfolípide

“…Azeem et al 7 described a case of EMF causing right heart failure in a 50-year-old patient that had APS. This type of cardiomyopathy still has an unknown etiology and is associated with several neurohumoral and growth factors 8 .…”

Cardiac Manifestations of Antiphospholipid Syndrome: Clinical Presentation, Role of Cardiac Imaging, and Treatment Strategies

“…Histologically proven inflammation areas, intramyocardial arterial immune deposition, and large coronary microvascular thrombosis are recognized determinants of myocardial fibrosis in APS. 61,62 Also, LV hypertrophy, a recognized determinant of LV diastolic dysfunction, could be involved. In patients with SLE and/or APS, the prevalence of LV hypertrophy has been found to be sixfold increased as compared to control subjects (32 vs. 5%, p < 0.005).…”