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Articles by Patrick M. Moriarty
Total Records ( 5 ) for Patrick M. Moriarty
  Anne C. Goldberg , Paul N. Hopkins , Peter P. Toth , Christie M. Ballantyne , Daniel J. Rader , Jennifer G. Robinson , Stephen R. Daniels , Samuel S. Gidding , Sarah D. de Ferranti , Matthew K. Ito , Mary P. McGowan , Patrick M. Moriarty , William C. Cromwell , Joyce L. Ross and Paul E. Ziajka
  The familial hypercholesterolemias (FH) are a group of genetic defects resulting in severe elevations of blood cholesterol levels and increased risk of premature coronary heart disease. FH is among the most commonly occurring congenital metabolic disorders. FH is a treatable disease. Aggressive lipid lowering is necessary to achieve the target LDL cholesterol reduction of at least 50% or more. Even greater target LDL cholesterol reductions may be necessary for FH patients who have other CHD risk factors. Despite the prevalence of this disease and the availability of effective treatment options, FH is both underdiagnosed and undertreated, particularly among children. Deficiencies in the diagnosis and treatment of FH indicate the need for greatly increased awareness and understanding of this disease, both on the part of the public and of healthcare practitioners. This document provides recommendations for the screening, diagnosis and treatment of FH in pediatric and adult patients developed by the National Lipid Association Expert Panel on Familial Hypercholesterolemia. This report goes beyond previously published guidelines by providing specific clinical guidance for the primary care clinician and lipid specialist with the goal of improving care of patients with FH and reducing their elevated risk for CHD.
  W. Virgil Brown , Robert Brook , Linda C. Hemphill and Patrick M. Moriarty
  Not available
  Patrick M. Moriarty , James Backes , Julie-Ann Dutton , Jianghua He , Janelle F. Ruisinger and Kristin Schmelzle
 

Background

Niacin, or vitamin B3, when used in high doses can significantly improve the levels of all major lipoproteins. Despite these benefits, the use of niacin is greatly limited secondary to benign yet bothersome cutaneous flushing primarily involving the face and upper extremities. Pretreatment with aspirin or other prostaglandin inhibitors has demonstrated significant reductions in niacin-induced flushing (NIF), but other treatment options are needed. Clinical and anecdotal evidence suggests the ingestion of pectin-containing fruits (eg, apple) mitigates NIF; however, clinical trials evaluating this are nonexistent.

Objective

That pretreatment with encapsulated apple pectin would limit the incidence, severity, time of initiation, and duration of NIF.

Methods

We enrolled 100 niacin-naive subjects (n = 25 per group) and preteated them in a double-blind manner with apple pectin, apple pectin + aspirin, aspirin, or placebo, followed by a one-time 1000 mg dose of niacin extended-release (niacin ER). Subjects then assessed major flushing parameters hourly for the next 6 hours with a validated visual analog scale.

Results

Apple pectin and aspirin each significantly lowered the duration of NIF and produced nonsignificant but positive improvements in all other major flushing parameters compared with placebo.

Conclusion

Apple pectin may potentially be an alternative to aspirin for the prevention of NIF. Larger trials are needed to further evaluate the benefit of pectin on NIF.

  James M. Backes , Cheryl A. Gibson , Janelle F. Ruisinger and Patrick M. Moriarty
 

Background

Alternative dosing is often used clinically to address common barriers with statin therapy, such as intolerance and cost. Previous findings have demonstrated significant and clinically similar reductions in low-density lipoprotein (LDL) cholesterol to daily dosing, when comparing similar total weekly doses.

Objective

To determine whether rosuvastatin 80 mg once weekly produced comparable lipid and high-sensitivity C-reactive protein (hsCRP) changes to atorvastatin 10 mg daily, when measured at key points after last dose.

Methods

This was a randomized, double-blind, parallel group, 8-week pilot study. Eligible subjects, 18 to 65 years of age, had documented dyslipidemia with LDL cholesterol >100 mg/dL and triglycerides <200 mg/dL. Participants were randomized to receive either rosuvastatin 80 mg once weekly (n = 10) or atorvastatin 10 mg daily (n = 10), for 8 weeks. Lipid panels and hsCRP were measured at baseline and 1-4 and 5-8 days after the last dose.

Results

Participants in each arm experienced significant and comparable reductions from baseline in total cholesterol, total cholesterol/high-density lipoprotein cholesterol ratio, non-high-density lipoprotein cholesterol, and overall LDL cholesterol (−29%). Changes in high-density lipoprotein cholesterol, triglycerides, and hsCRP were nonsignificant and similar between groups. Each regimen was well tolerated, with no major adverse events reported.

Conclusion

Rosuvastatin 80 mg once weekly produced comparable lipid changes to atorvastatin 10 mg daily when measured at specific points after the last dose. Our findings support previous data demonstrating a significant reduction in LDL-C with once weekly statin dosing.

  James M. Backes , Thomas Dayspring , Thomas Mieras and Patrick M. Moriarty
  The National Cholesterol Educational Program Adult Treatment Panel's third report define borderline-high, high, and very high triglycerides as serum levels of 150-199 mg/dL, 200-499 mg/dL, and ≥500 mg/dL, respectively. Hypertriglyceridemia (HTG) is generally very responsive to both therapeutic lifestyle changes (TLC), and drug therapy, with niacin, omega-3 fatty acids, fibrates, and statins, each reducing levels by ∼10-50%. This paper presents two cases of patients who were aggressively treated for significant HTG with little response to therapy. Although most measured triglyceride (TG) values in these patients were markedly elevated, periodic concentrations were reported as normal. When this occurs, the clinician must immediately think of the diagnosis ‘pseudohypertriglyceridemia’ or as it is more aptly termed ‘glycerolemia’ secondary to glycerol kinase deficiency (GKD).
 
 
 
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