Closing Gaps in Lifestyle Adherence for Secondary Prevention of Coronary Heart Disease.

The secondary prevention (SP) of coronary heart disease (CHD) has become a major public health and economic burden worldwide. In the United States, the prevalence of CHD has risen to 18 million, the incidence of recurrent myocardial infarctions (MI) remains high, and related healthcare costs are projected to double by 2035. In the last decade, practice guidelines and performance measures for the SP of CHD have increasingly emphasized evidence-based lifestyle (LS) interventions, including healthy dietary patterns, regular exercise, smoking cessation, weight management, depression screening, and enrollment in cardiac rehabilitation. However, data show large gaps in adherence to healthy LS behaviors and low rates of enrollment in cardiac rehabilitation in patients with established CHD. These gaps may be related, since behavior change interventions have not been well integrated into traditional ambulatory care models in the United States. The chronic care model, an evidence-based practice framework that incorporates clinical decision support, self-management support, team-care delivery and other strategies for delivering chronic care is well suited for both chronic CHD management and prevention interventions, including those related to behavior change. This article reviews the evidence base for LS interventions for the SP of CHD, discusses current gaps in adherence, and presents strategies for closing these gaps via evidence-based and emerging interventions that are conceptually aligned with the elements of the chronic care model.

A Clinician's Guide for Trending Cardiovascular Nutrition Controversies: Part II.

The potential cardiovascular (CV) benefits of many trending foods and dietary patterns are still incompletely understood, and scientific inquiry continues to evolve. In the meantime, however, a number of controversial dietary patterns, foods, and nutrients have received significant media attention and are mired by "hype." This second review addresses some of the more recent popular foods and dietary patterns that are recommended for CV health to provide clinicians with current information for patient discussions in the clinical setting. Specifically, this paper delves into dairy products, added sugars, legumes, coffee, tea, alcoholic beverages, energy drinks, mushrooms, fermented foods, seaweed, plant and marine-derived omega-3-fatty acids, and vitamin B12.

Guanidinoacetate methyltransferase deficiency (GAMT).

An increasing number of disorders of metabolism are becoming amenable to the treatment, and GAMT deficiency is one of them. The symptoms and signs are reviewed, emphasising that delayed language development is a particular feature. Other symptoms include learning disorders, autistic behaviour, epileptic seizures, and movement disorders. The condition is inherited in an autosomal recessive manner, and mutations in the GAMT gene severely affect the activity of guanidinoacetate. The MRI scan shows an increased signal in the globus pallidus, and the diagnosis is confirmed by finding increased guanidinoacetate in the urine and a low plasma creatine. Other methods of diagnosis are discussed. Treatment is based on giving creatine supplementation orally and a low-protein diet with restricted arginine and increased ornithine. This results in improvement of many of the symptoms, especially of the epileptic seizures and the abnormal movements. It is justifiable to consider this condition in any patient with unexplained learning disorders.

Glutaric aciduria types I and II.

Glutaric aciduria type I is an autosomal recessive disorder resulting from a deficiency of glutaryl-CoA dehydrogenase. This leads to an accumulation of glutaric and 3-hydroxyglutaric acids and secondary carnitine deficiency. The symptomatology is discussed, especially those resulting from lesions in the basal ganglia, and the encephalopathic episodes which are often precipitated by infections. The variability of the clinical presentation is stressed. The most serious complications are collections of fluid and blood in the middle fossae, the bleeding resulting from rupture of bridging veins. The prognosis does not seem to be related to the extent of the enzyme deficiency. The diagnosis is confirmed by identifying the abnormal acids in the urine and the deficiency of the enzyme in cultured fibroblasts. The differential diagnosis is reviewed: from other biochemical disorders and from other cerebral lesions. Treatment is by special diet and carnitine supplementation. The dystonia can prove difficult to treat, and surgery may be needed to remove the collections of fluid and blood. Glutaric aciduria type II is caused by a deficiency of either electron transport flavoprotein or of electron transport flavoprotein oxoreductase. The symptoms can be mild or severe. The former may only occur in times of stress, and the latter include congenital anomalies, especially of the kidneys and heart. The pathology of these are discussed. The demonstration of organic acids in the urine and the results of muscle and liver biopsies confirm the diagnosis, and treatment with a special diet and supplementation with carnitine and riboflavine is effective.