Further information: Coronary Risk Factors: An Overview (see p2609) from Cardiovascular Medicine, 3rd Edn*

The Clinical Guidelines section of the October 6, 2009 issue of Annals of Internal Medicine contained three articles reporting the recommendations of the United States Preventive Services Task Force (USPSTF) regarding the addition of non-traditional risk factors in determining patients’ risk for coronary heart disease (CHD). This review summarizes the paper reporting on the use of C-reactive protein (CRP) [1].

Forty percent of deaths in the US can be attributed to cardiovascular (CV) disease  and, although Framingham risk factors can be attributed to most of the excessive risk for coronary heart disease (CHD), an estimated 40% of CHD deaths occur in people who do not have high cholesterol or other elements of the Framingham risk score. With increasing awareness, chronic inflammation in CHD has been targeted as a major factor in CHD risk, and therefore, the role of inflammatory marker, CRP, has come under scrutiny. In particular, the current article addresses whether or not the routine measurement of CRP is a beneficial marker for risk of death from CHD.

From articles published between 1966 and November 2007, the authors of this study selected prospective, cohort, case-cohort, and nested case-cohort studies that pertained to the independent predictive ability of CRP used in intermediate-risk patients. The review was conducted to help the USPSTF determine whether a test for a patient’s CRP level should be incorporated into guidelines for CV risk assessment in primary care testing. Investigators concluded that although the study found evidence that CRP is associated with CHD, the evidence that proves reducing CRP prevents CHD is not conclusive.

[1] Buckley DL, Fu R, Freeman M, et al. C-reactive protein as a risk factor for coronary artery disease: a systematic review and meta-analyses for the U.S. preventive Services task force. Ann Intern Med 2009;151:483-95.

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Further information: Cardiovascular Complications of Obesity and the Metabolic Syndrome (see p2693) from Cardiovascular Medicine, 3rd Edn*

The goal of investigators in this study [1] was to determine the mechanisms by which leptin, an adipocyte-derived hormone that is increased in most forms of obesity, affects cardiovascular function. In addition to leptin’s communicating to the central nervous system in regard appetite and metabolism, its signaling pathways communicate to the sympathetic nervous system. Protein tyrosine phosphate 1B (PTP1B), as a regulator of this signaling pathway, constrains the metabolic activity of leptin. Pharmacological efforts are underway to develop PTP1B inhibitors for the treatment of metabolic disorders, but in the present study, the PTP1B knockout mice under observation had lower body fat, but higher mean arterial pressure from an increased sympathetic affect on blood pressure.

In an accompanying Editorial [2], Dr Mark comments on the recent identification of new pathways that regulate appetite and metabolism, pathways that also affect the regulation of sympathetic neural activity and arterial pressure. In relationship to the current study [1] that shows adverse sympathetic and arterial pressure responses to genetic deletion of the leptin and insulin inhibitor PTP1B in knockout mice, Dr. Mark explains that while leptin does act in the brain to decrease adiposity, its pleiotropic effect also influences arterial pressure regulation. Therefore, he noted that this complicated the safety of antiobesity drugs and emphasized the importance of evaluating the cardiovascular actions of these potentially emerging drugs.

[1] Belin de Chantemele EJ, Muta K, Mintz J, et al. Protein tyrosine phosphatase 1B, a major regulator of leptin-mediated control of cardiovascular function. Circulation 2009;120:753-63

[2] Mark AL. Cardiovascular side effects of antiobesity drugs. Circulation 2009;120:719-21

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Further information: Treatment of Acute ST-Elevation Myocardial Infarction (see p963) and Sudden Cardiac Death (see p2039) from Cardiovascular Medicine, 3rd Edn*

Investigators for the Immediate Risk Stratification Improves Survival (IRIS) trial sought to prove that when compared to optimal medical therapy after myocardial infarction (MI), early implantation of an implantable cardioverter-defibrillator (ICD) would improve survival of patients at risk of sudden death [1]. The trial was a multicenter, randomized, prospective trial that was investigator-initiated and open-label. From a total of 62,944 patients registered with MI between June 1999 and October 2007, 898 patients met the criteria for enrollment 5–31 days after the event. Of those, 453 were randomized to medical therapy alone and 445 to treatment with an ICD. Overall mortality was not reduced in the ICD group, although there were fewer sudden cardiac deaths ( 27 vs. 60; hazard ratio [HR], 0.55; 95% confidence interval [CI], 0.31–1.00; P=0.049). The number of cardiac deaths that were not sudden death was higher (68 vs. 39; HR, 1.92; 95% CI, 1.29–2.84; P=0.001). Investigators concluded that no evidence was found to substantiate that early implantation of an ICD improved survival in patients with acute MI who had clinical features that put them at increased risk of sudden death.

[1] Steinbeck G, Andresen D, Seidl K, et al. Defibrillator implantation early after myocardial infarction. N Engl J Med 2009;361:1427-1436

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* To view the online text from the book, please navigate to SpringerLink or use the DVD to access electronic content. SpringerLink is a subscription service. For further information, click here.