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Kathleen Maksimowicz-McKinnon

Publications and source records attributed to Kathleen Maksimowicz-McKinnon.

6 recordsLinked to original sources
PubMed2006

Predictors of carotid atherosclerosis in systemic lupus erythematosus.

OBJECTIVE: Patients with systemic lupus erythematosus (SLE) are at increased risk for cardiovascular and cerebrovascular events, even after adjustment for traditional risk factors. We examined the association of traditional risk factors, novel markers of cardiovascular disease (C-reactive protein, homocysteine, lipoprotein(a), plasminogen activator inhibitor-1, fibrinogen), and markers indicative of SLE activity (including C3, C4, anti-dsDNA, and prednisone use) with the presence of significant plaque on carotid duplex imaging. METHODS: Six hundred five patients with SLE enrolled in the Hopkins Lupus Cohort Study (92% female, 38% African-American) underwent carotid duplex testing. Prospectively gathered clinical, laboratory, and serologic data from their quarterly followup visits in the Hopkins Lupus Cohort were used in the analyses. For predictors that varied over time, such as cholesterol, the mean values during cohort participation were calculated for the analysis. Informed consent was obtained from all patients. RESULTS: The presence of carotid plaque was strongly associated with age, ranging from 1% among those less than 30 years of age to 61% among those 60 years or older. After adjusting for age, there were moderate or strong associations of carotid plaque with male gender (age-adjusted risk 25% vs 13%; p = 0.051), hypertension (age-adjusted risk 18% vs 8%; p = 0.0001), diabetes mellitus (age-adjusted risk 19% vs 13%; p = 0.075), C3 > 120 mg/dl (age-adjusted risk 18% vs 11% and 14% for normal and low C3, respectively; p = 0.046), serum creatinine > 1.3 (age-adjusted risk 32% vs 13%; p = 0.039), and mean systolic blood pressure > 140 (age-adjusted risk 23% vs 13%; p = 0.028). There was no strong evidence of an association between plaque and SLE disease activity (age-adjusted risk 14% among those with adjusted mean SLEDAI > 3 vs 14% among those with lower SLEDAI) or with time since SLE diagnosis (age-adjusted risk 12%, 14%, and 16% among those with SLE for < 2, 2-8, and > 8 years, respectively; p = 0.49). CONCLUSION: Traditional cardiovascular risk factors were associated with carotid plaque in SLE. However, SLE disease activity and duration of SLE are not strongly associated with carotid plaque. A "lupus factor" separate from traditional risk factors remains unidentified.

Adult↗
PubMed2006

Prevention of cardiovascular disease in patients with rheumatic diseases.

Cardiovascular disease (CVD), the leading cause of death in the USA, has emerged as an important comorbidity in the rheumatic diseases. As disease-modifying therapies have resulted in better disease control and decreases in disease-associated mortality, it is now apparent that the prevalence of CVD and cardiovascular (CV) events is significantly increased in a number of rheumatic disorders when compared with age and gender-matched subjects from the general population. Investigations into the mechanisms of CVD in the general population have provided insights into potential mechanisms in rheumatic disease patients and possible aetiologies for their increased risk. Although there are no evidence-based guidelines for CV risk factor screening and interventions specific to patients with rheumatic disease, the best current approach utilizes evidence-based recommendations for the general population (and higher-risk subgroups) modified by what is known of CV risk factor and event prevalence in these patients.

Cardiovascular Diseases↗
PubMed2004

Large-vessel vasculitis.

The vasculitides affecting large and medium-sized vessels are heterogeneous. This group includes such disorders as giant cell arteritis, Takayasu's disease, and sarcoidosis. There are several challenges that may arise in the care of patients with these disorders. Diagnosis may be elusive when initially evaluating patients with large-vessel vasculitis. Most serologic markers are not specific, and tissue biopsy is often impractical. We will present data emphasizing the most common disease manifestations, to aid in recognition of a clinical picture suggestive of large-vessel vasculitis. We will also focus on the more common pulmonary manifestations and minimize case reports, which may not reflect the usual course of disease. Large cohort studies and randomized controlled trials to provide an evidence-based approach to therapy in these disorders are uncommon. We have included in this review discussion of those studies that we judged to be most rigorously conducted and clinically relevant. We provide guidelines for initial therapy, with caveats to assist in minimizing potential treatment-related complications and toxicities. Although monitoring of disease activity is often difficult, this is a most crucial element in minimizing disease and treatment-associated morbidity and mortality.

Journal Article↗
PubMed2004

Recent advances in vascular inflammation: C-reactive protein and other inflammatory biomarkers.

PURPOSE OF REVIEW: Inflammatory vascular diseases are initiated and perpetuated by the interaction of immune cells with cells of the affected vessel wall. This is directed by a network of chemical messengers, which, in a state of vascular health, exist as balanced but opposing forces. Our understanding of this highly complex process has advanced significantly in the last several decades. The detection of vascular inflammation and monitoring of this activity have long been attempted in systemic vasculitis, and, more recently, in atherosclerosis. Markers of vascular inflammation used thus far have been of limited value; few provide both adequate sensitivity and specificity for any particular disease. New insights into the pathophysiology of vascular inflammation have identified other potential markers that may improve detection and monitoring of these conditions. RECENT FINDINGS: Immunomodulatory mediators of the inflammatory cascade have been identified, and their roles are being defined. There are recent data that implicate various cytokines, proteases, adhesion molecules, and acute phase proteins as participants in the generation of vascular inflammation. CONCLUSION: The pursuit of highly sensitive and specific markers of vascular inflammation has produced a wealth of information that has been instrumental in advancing our comprehension of this complex process. Further studies will establish the role of these new markers in the diagnosis, monitoring, and prognostication of inflammatory vascular disease.

Biomarkers↗