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W orldwide, cardiovascular disease (CVD) is the largest single cause of death among women, accounting for one third of all deaths. 1 In many countries, including the United States, more women than men die every year of CVD, a fact largely unknown by physicians. 2,3 The public health impact of CVD in women is not related solely to the mortality rate, given that advances in science and medicine allow many women to survive heart disease. For example, in the United States, 38.2 million women (34%) are living with CVD, and the population at risk is even larger. 2 In China, a country with a population of approximately 1.3 billion, the agestandardized prevalence rates of dyslipidemia and hypertension in women 35 to 74 years of age are 53% and 25%, respectively, which underscores the enormity of CVD as a global health issue and the need for prevention of risk factors in the first place. 4 As life expectancy continues to increase and economies become more industrialized, the burden of CVD on women and the global economy will continue to increase. 5 The human toll and economic impact of CVD are difficult to overstate. In the United States alone, $403 billion was estimated to be spent in 2006 on health care or in lost †Representation does not imply endorsement by the American College of Physicians. The online-only Data Supplement is available with this article at http://circ.ahajournals.org/cgi/content/full/CIRCULATIONAHA.107.181546/DC1. The American Heart Association makes every effort to avoid any actual or potential conflicts of interest that may arise as a result of an outside relationship or a personal, professional, or business interest of a member of the writing panel. Specifically, all members of the writing group are required to complete and submit a Disclosure Questionnaire showing all such relationships that might be perceived as real or potential conflicts of interest.This statement was approved by the American Heart Association Science Advisory and Coordinating Committee on January 9, 2007. A single reprint is available by calling 800-242-8721 (US only) or writing the American Heart Association, Public Information, 7272 Greenville Ave, Dallas, TX 75231-4596. Ask for reprint No. 71-0401. To purchase additional reprints, call 843-216-2533 or e-mail kelle.ramsay@wolterskluwer.com.This article has been copublished in the March 20, 2007, issue of the Journal of the American College of Cardiology. Expert peer review of AHA Scientific Statements is conducted at the AHA National Center. For more on AHA statements and guidelines development, visit http://www.americanheart.org/presenter.jhtml?identifierϭ3023366.Permissions: Multiple copies, modification, alteration, enhancement, and/or distribution of this document are not permitted without the express permission of the American Heart Association. Instructions for obtaining permission are located at http://www.americanheart.org/presenter.jhtml? Identifierϭ4431. A link to the "Permission Request Form" appears on the right side of the page.( Fortunately, most CVD in wome...

W orldwide, cardiovascular disease (CVD) is the largest single cause of death among women, accounting for one third of all deaths (1). In many countries, including the United States, more women than men die every year of CVD, a fact largely unknown by physicians (2,3). The public health impact of CVD in women is not related solely to the mortality rate, given that advances in science and medicine allow many women to survive heart disease. For example, in the United States, 38.2 million women (34%) are living with CVD, and the population at risk is even larger (2). In China, a country with a population of approximately 1.3 billion, the agestandardized prevalence rates of dyslipidemia and hypertension in women 35 to 74 years of age are 53% and 25%, respectively, which underscores the enormity of CVD as a †Representation does not imply endorsement by the American College of Physicians. Please see the online version of this document for data supplements. The American Heart Association makes every effort to avoid any actual or potential conflicts of interest that may arise as a result of an outside relationship or a personal, professional, or business interest of a member of the writing panel. Specifically, all members of the writing group are required to complete and submit a Disclosure Questionnaire showing all such relationships that might be perceived as real or potential conflicts of interest.

Abstract-Chronic kidney disease (CKD) occurs commonly in patients with cardiovascular disease. In addition, CKD is a risk factor for the development and progression of cardiovascular disease. In this advisory, we present recommendations for the detection of CKD in patients with cardiovascular disease. CKD can be reliably detected with the combined use of the Modification of Diet in Renal Disease equation to estimate glomerular filtration rate and a sensitive test to detect microalbuminuria. All patients with cardiovascular disease should be screened for evidence of kidney disease with these two determinations.

The effect of cytosolic free Mg2+ concentration on the regulation of myocardial function was studied by dialyzing isolated guinea pig ventricular myocytes with different internal Mg2+ concentrations [( Mg2+]i). We found that elevation of [Mg2+]i shortened the action potential and suppressed the Ca2+ current. Mean values recorded for action potential duration in cells dialyzed with solutions containing 0, 1.3, and 9.4 mM Mg2+ were 620 +/- 40, 400 +/- 25, and 60 +/- 10, respectively. The suppressive effect of [Mg2+]i on the action potential duration correlated significantly with the suppressive effects of [Mg2+]i on the Ca2+ current. In cells dialyzed with nominally zero Mg2+, calcium current was prominent (3.5 +/- 0.58 nA). At [Mg2+]i of 1.4 mM, calcium current was significantly smaller than in zero [Mg2+]i and was almost completely inhibited by dialysis of the cell with 9.4 mM Mg2+. The Mg2+-induced block of the Ca2+ current was due to steady-state inactivation of the high threshold calcium channel. The block was observed in the presence or absence of adenosine 3',5'-cylic monophosphate and was not reversed by elevation of external Ca2+ concentration, addition of adrenaline, or large negative potentials. These data suggest that cytosolic Mg2+ regulates Ca2+ channel activity by a novel mechanism, unrelated to its effect as a blocking particle of the open channel.