A Call to Action: Responding to the Future Forecasting of Cardiovascular Disease in America

Background

Cardiovascular disease (CVD) continues to be a leading cost driver for payers in the United States.1 The American Heart Association estimates that more than 75 million individuals nationwide have some form of CVD. Individuals aged 20 to 45 years are developing CVD at higher rates than ever before.

Objectives

To discuss the alarming increase in the rate of CVD in young adults (aged 18–45 years) previously only seen in older adults (aged ≥65 years) and describe the 5 primary risk factors (smoking, obesity, hypertension, diabetes, and dyslipidemia) that contribute to this new trend in the working-age population.

Discussion

Using Medical Expenditure Panel Survey data, this article outlines the increased prevalence of the 3 primary components of CVD—stroke, heart failure, and myocardial infarction—in younger adults and the cost impact on payers and on US society. The examples provided in this article highlight the need for increased efforts by all healthcare stakeholders, and by payers in particular, to develop prevention strategies for CVD risk factors targeted at young adults to curb the alarming rise in CVD among this age-group.

Conclusion

This article provides compelling evidence for the need to institute prevention measures to curb the growing prevalence of CVD risk factors among younger adults in the United States.Despite advances in life-saving medical interventions and pharmacotherapies, cardiovascular disease (CVD) continues to be a leading killer in the United States.1 The spectrum of CVD consists of hypertension, chronic heart disease (CHD; including myocardial infarction [MI] and angina), heart failure, and stroke. Based on 2009 data from the American Heart Association (AHA), 76.4 million Americans have been diagnosed with hypertension, 16.3 million have CHD, 5.7 million have heart failure, and 7 million have stroke.2Beginning in adolescence, CVD can stay dormant for many years before emerging in adulthood. Among each of the components of CVD, CHD accounts for 1 in every 6 American deaths, heart failure for 1 in every 9 deaths, and stroke for 1 in every 18 deaths.2Despite these dramatic statistics, CVD mortality rates have begun to decline over the past decade (Figure 1).2,3 These reductions are primarily a result of advances in medical and interventional therapies, as well as to increased acceptance and application of evidence-based guidelines.2,3 In addition, over the past decade the AHA and the American College of Cardiology (ACC) have launched nationwide campaigns that incentivize health systems to improve the overall quality of hospital care through the implementation of CVD quality core measures. Recently, a large population-based study suggested that the age- and sex-adjusted incidence of acute MI exhibited a 24% relative decrease between 1999 and 2008 and that the age- and sex-adjusted 30-day mortality rate after acute MI decreased from 10.5% in 1999 to 7.8% in 2008 (P <.001).4Open in a separate windowFigure 1US Deaths from Diseases of the Heart, 1900–2007NOTE: The vertical line marks the beginning in the decline of deaths from heart disease.Adapted with permission from Roger VL, et al. Circulation. 2011;123:e18-e209.     

Anaplastic carcinoma of the thyroid: A 24-year experience

Background. Anaplastic carcinoma of the thyroid gland is a lethal entity; few patients live more than 12 months following diagnosis. We retrospectively reviewed the experience with this entity at our cancer institute and identified a subgroup of patients with complete resection who have a 60% 5-year survival. Methods. Twenty-one cases of anaplastic carcinoma of the thyroid gland were analyzed retorspectively with respect to prognostic factors influencing survival. This represents 2.7% of 771 cases of thyroid cancer seen at our institution from 1968 to 1992. The median age at presentation was 65.1 years; male/female ratio was 1:1.1; and the most common symptom was a rapidly enlarging neck mass (76%). Results. Estimated 5-year survival was 10% (median: 4.5 months). Tumor size less than 6.0 cm (p = .004) and female gender (p = .02) were significant prognostic factors. Five patients who underwent complete resection had an estimated 5-year survival of 60% (median: 131 months). Four of these patients had postoperative radiotherapy with or without sequential chemotherapy. Two of these patients survived more than 10 years, and a third remains alive without disease at 26 months. Conclusions. Complete resection and multimodality therapy result in long-term survival for a subgroup of patients with anaplastic thyroid carcinoma. © 1995 Jons Wiley & Sons, Inc.     

Cognitive burden and excess Lewy-body pathology in the Lewy-body variant of Alzheimer disease.

OBJECTIVES: Authors compared the degrees of cognitive deficit among individuals with Alzheimer disease (AD), the Lewy-body variant of AD (LBV), and "pure" dementia with Lewy bodies (DLB); and compared cortical Lewy body (LB) counts in LBV versus DLB and neuritic plaque and neurofibrillary tangle severity in LBV versus AD. METHODS: Authors examined brain specimens from consecutive autopsies of elderly nursing home subjects. Numbers and densities of plaques, Lewy bodies, and tangle severity were determined in multiple cortical regions, and demographic and clinical variables were compared among the three groups. RESULTS: The three groups did not differ in demographic or clinical variables. The LBV group was significantly more impaired than the other groups. Cortical LB counts were significantly higher in LBV than in DLB. There was no evidence of increased plaque or tangle severity in LBV than in AD. CONCLUSION: The co-occurrence of AD and LB pathology is associated with higher numbers of LBs and more severe dementia than when classical AD or LB lesions occur alone.     

Dementia rating and nicotinic receptor expression in the prefrontal cortex in schizophrenia.

BACKGROUND: The etiology of dementia that occurs in patients with schizophrenia is not well understood. Nicotinic acetylcholine receptors have been implicated in cognitive function, and deficits in these receptors have been reported in schizophrenia. METHODS: The present study investigates possible associations of nicotinic receptor subunit expression in the dorsal lateral prefrontal cortex, an area known to be affected in schizophrenia, and dementia rating. RESULTS: alpha7 immunoreactivity was reduced by 20% to 28% and [(3)H]epibatidine binding was increased twofold in groups of patients with schizophrenia compared to normal control subjects matched for age, postmortem delay, and low levels of brain nicotine and cotinine. In contrast, no significant differences in alpha4, alpha3, or beta2 immunoreactivity or alpha7 messenger RNA expression were observed in schizophrenia patients compared with control subject values. Clinical dementia ratings in patients with schizophrenia were correlated with neither [(3)H]epibatidine binding nor nicotinic receptor subunit expression. CONCLUSIONS:These data indicate no relationship between the trend for reduced neocortical alpha7 subunit protein expression in schizophrenia and dementia. Further investigations are required to establish whether the reduction in alpha7 protein in the dorsal lateral prefrontal cortex is associated with clinical features other than dementia in schizophrenia.     

Regional differences in expression of β-tubulin isoforms in schizophrenia

A growing body of evidence suggests that abnormal elements of the cytoskeleton may be associated with the pathophysiology of schizophrenia. Isoforms of a major cytoskeleton protein, β-tubulin, were recently demonstrated to have distinct roles in neuronal differentiation and cell viability. For these reasons, we tested the hypothesis that there are differences in the expression of β-tubulin isoforms (βI-βIV) in the brain in schizophrenia, using western blot analysis in an elderly group of subjects with this illness and a control group. We found that βI-tubulin protein expression was decreased in the anterior cingulate cortex and increased in the dorsolateral prefrontal cortex, but not changed in superior temporal gyrus or hippocampus in schizophrenia. Our data supports the growing body of evidence suggesting abnormalities of the cytoskeleton in schizophrenia.     

Expression of equilibrative nucleoside transporter type 1 protein in elderly patients with schizophrenia

Alterations in glutamatergic neurotransmission are thought to be involved in several psychiatric disorders, including schizophrenia. Equilibrative nucleoside transporter type 1 (ENT1) regulates glutamate levels by regulating excitatory amino acid transporter expression and activity in the brain. In this study, we investigated whether ENT1 is abnormally expressed in the brain of elderly patients with schizophrenia. We measured protein expression of ENT1 in the superior temporal gyrus (STG) and anterior cingulate cortex (ACC) in patients with schizophrenia (STG, n=22; ACC, n=34) and a comparison group (STG, n=24; ACC, n=29). We found decreased ENT1 expression in the STG in patients with schizophrenia, supporting the hypothesis of altered glutamate transport in this illness.     

Convergent evidence for 2',3'-cyclic nucleotide 3'-phosphodiesterase as a possible susceptibility gene for schizophrenia

CONTEXT: Convergent data make 2',3'-cyclic nucleotide 3'-phosphodiesterase (CNP) a candidate gene for schizophrenia. Reduced expression has been reported in the schizophrenic brain. The CNP gene maps to a region to which we have reported linkage to schizophrenia. Mice in which the CNP gene has been knocked out display central nervous system pathological characteristics reminiscent of some features observed in schizophrenia. 2',3'-Cyclic nucleotide 3'-phosphodiesterase is used as a marker of myelin-forming cells and is detectable in cells of oligodendrocyte lineage throughout life. Because CNP is thought to be important for oligodendrocyte function, altered expression has been interpreted as supportive of the hypothesis that altered oligodendrocyte function may be an etiological factor in schizophrenia. However, it is unclear whether the observed changes in the schizophrenic brain are primary or secondary. OBJECTIVES: To determine if CNP expression is influenced by DNA polymorphisms and to verify if these polymorphisms are associated with schizophrenia. DESIGN: Allele-specific messenger RNA expression assay and genetic association studies. SETTING: Unrelated subjects were ascertained from secondary psychiatric inpatient and outpatient services. PARTICIPANTS: We used brain tissue from 60 anonymous individuals with no known psychiatric disorder; a case-control sample of 708 white individuals from the United Kingdom meeting DSM-IV criteria for schizophrenia matched for age, sex, and ethnicity to 711 blood donor controls; and a pedigree with DNA from 6 affected siblings and 1 parent, showing evidence for linkage to CNP. MAIN OUTCOME MEASURES: Association between allele and gene expression. Association between allele and schizophrenia. RESULTS: The exonic single nucleotide polymorphism rs2070106 was associated with CNP expression (P<.001). Compatible with underexpression of CNP messenger RNA in schizophrenia, the lower-expressing A allele was significantly associated with schizophrenia (P = .04) in the case-control sample. All affected individuals in the linked pedigree were homozygous for the lower-expression allele, providing independent support for the association (P = .03). CONCLUSIONS: Our data support the hypothesis that reduced CNP expression in the schizophrenic brain is relevant to disease etiology and therefore provide support for the general hypothesis that altered oligodendrocyte function is an etiological factor in schizophrenia.