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J. Bill McEvoy, MB BCh, MHS

Ciccarone Center Research

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J. Bill McEvoy, MB BCh, MHS

J. Bill McEvoy, MB BCh, MHS
McEvoy, J. Bill, MB BCH, MHS

J. Bill McEvoy, MB BCH, MHS, is an Assistant Professor of Medicine.

Landmark Articles

Metabolically benign obesity: a wolf in sheep’s clothing.

Schnitzler’s syndrome associated with pancreatitis: a disease of IL-1 dysregulation.

By: Larocca CA, McEvoy JW, Ellis CL, Junkins-Hopkins J, Kolb T, Baer AN, Garibaldi BT.
Schnitzler's syndrome (SS) is a rare inflammatory disease of unknown origin characterized by chronic urticaria and monoclonal gammopathy (usually IgM) associated with at least two of the following components: fever, arthralgia or arthritis, bone pain, hepato- and/or splenomegaly, lymphadenopathy, elevated erythrocyte sedimentation rate, leukocytosis, and/or abnormal findings on bone morphological investigations. To date, about 100 cases have been described with only 4 being reported in the USA. The mean time to diagnosis from the onset of disease is 5.4 years, given the varied symptoms with which patients may present. The pathogenesis of SS remains unknown but likely involves dysregulation of the IL-1 pathway. We describe here a 48-year-old woman with a monoclonal IgM gammopathy and a 3-year history of chronic pruritic urticarial dermatosis, unexplained fevers, chronic polyarthritis, lymphadenopathy, leukocytosis, hepatomegaly, and weight loss. She also had a history of chronic pancreatitis as well as a family history of recurrent pancreatitis. The diagnosis of Schnitzler's syndrome was made, and she was successfully treated with the IL-1 receptor antagonist, anakinra.
Read on Pubmed

Letter regarding “Pathogenesis of sudden unexpected death in a clinical trial of patients with myocardial infarction and left ventricular dysfunction, heart failure, or both.

By: McEvoy JW.

Coronary artery calcium progression: an important clinical measurement? A review of published reports.

By: McEvoy JW, Blaha MJ, Defilippis AP, Budoff MJ, Nasir K, Blumenthal RS, Jones SR.
Baseline CAC accurately identifies coronary atherosclerosis and improves prediction of future cardiac events. However, whether knowledge of progression of CAC scores over time further improves risk prediction is unclear. We conducted a comprehensive review of published reports on CAC progression and found that CAC progression correlates with worsening atherosclerosis and may facilitate prediction of future cardiac events. These findings support the notion that slowing CAC progression with therapeutic interventions might provide prognostic benefit. However, despite promising early data, such interventions (most notably with statin therapy) have not been shown to slow the progression of CAC in any randomized controlled trial to date, outside of post hoc subgroup analyses. Thus, routine quantification of CAC progression cannot currently be recommended in clinical practice.

Coronary artery calcium progression — an important clinical measurement? (State of the Art Paper)

By: McEvoy JW, Blaha M, DeFilippis A, Budoff M, Nasir K, Blumenthal RS, Jones SR.

Baseline coronary artery calcification (CAC) accurately identifies coronary atherosclerosis and might improve prediction of future cardiac events. Serial assessment of CAC scores has been proposed for monitoring atherosclerosis progression and for assessing the effectiveness of medical therapies aimed at reducing cardiac risk. However, whether knowledge of progression of CAC scores over time further improves risk prediction is unclear. Several trials relating medical therapies to CAC progression have been performed without any formal guidelines on the definition of CAC progression and how it is best quantified. We conducted a comprehensive review of published reports on CAC progression. Increased CAC progression is associated with many known cardiac risk factors. We found that CAC progression correlates with worsening atherosclerosis and may facilitate prediction of future cardiac events. These findings support the notion that slowing CAC progression with therapeutic interventions might provide prognostic benefit. However, despite promising early data, such interventions (most notably with statin therapy) have not been shown to slow the progression of CAC in any randomized controlled trial to date, outside of post hoc subgroup analyses. Thus, routine quantification of CAC progression cannot currently be recommended in clinical practice. First, standards of how CAC progression should be defined and assessed need to be developed. In addition, there remains a need for further studies analyzing the effect of other cardiac therapies on CAC progression and cardiac outcomes.

Coronary artery calcium score and cardiovascular event prediction.

By: McEvoy JW.
In the study by Polonsky et al, the net reclassification index (NRI) for CHD (myocardial infarction, cardiac death, resuscitated arrest, and definite angina) was +25% overall. However, 24 of 209 patients who experienced events (11%) were reclassified to a lower risk group by calcium scoring. As the authors point out, a randomized controlled trial is needed to assess the use of coronary artery calcium score (CACS) reclassification on clinical outcomes. This current study is a compelling argument to provide support for such an endeavor.

Caveat emptor: the coronary calcium warranty.

By: McEvoy JW, Blaha MJ, Blumenthal RS.
It would be beneficial for clinicians to have the “warranty period” of a zero coronary calcium score stratified by baseline risk group (<10% and 10% to 20%). It may even be prudent to stratify further, as some have advocated for CAC testing in an expanded intermediate-risk group of 6% to 20% (e.g., <6%, 6% to 10%, and 10% to 20%). The investigators may have been overly prudent to suggest that “caution should be applied to interpreting our results among patients who are not receiving lipid-lowering therapy.” Although they express concern that the 756 patients on statin therapy (72%) may have had retarded CAC progression, randomized trials to date have not shown that statin therapy can achieve this. CAC = 0 has enormous potential for ruling out important coronary artery disease in asymptomatic patients. The duration and application of the “warranty period” remains an important topic for further research.

What is the prognostic value of a zero calcium score? Ask Bayes!

By: McEvoy JW.
The role of calcium scoring (CS), if any, appears to be in the reclassification of asymptomatic patients at intermediate risk for CAD by traditional risk factor models. This has led to a Class IIb recommendation by the American Heart Association for the use of CS in these patients. Further research is ongoing to study the effect of such reclassification.

Statins and risk of incident diabetes.

By: McEvoy JW.

Reported limitations of a meta-analysis of whether statin therapy affects incident diabetes (13 statin trials with 91,140 participants) include the loss of statistical significance on exclusion of two trials in which incident diabetes was by physician report only. Post-hoc and subgroup analyses introduce analytical errors that can lead to misleading conclusions. Therefore, these capricious findings should be regarded as a hypothesis generating statistical anomaly, lest we fall foul of the logical fallacy, “Post hoc ergo propter hoc.”

Progression of coronary artery calcification: not down-and-out.

By: McEvoy JW, Blaha MJ.

Blood pressure has been consistently shown to be strongly associated with CAC progression, and we believe that the findings of INSIGHT (International Nifedipine Study: Intervention as Goal for Hypertension Therapy) are diluted by inclusion in the heterogeneous review by McCullough et al. Unfortunately, on-treatment blood pressure control was not reported in this trial. We look forward to seeing the results of future blood pressure and CAC progression trials before agreeing with the authors’ conclusion that CAC “may not be a suitable surrogate target for treatment trials in patients with cardiovascular or renal disease.”