Jeffrey L. Anderson, MD, FACC, FAHA, Chair 

Jonathan L. Halperin, MD, FACC, FAHA, Chair-Elect 

Alice K. Jacobs, MD, FACC, FAHA, Immediate Past Chair 2009–2011 [§§][1]

Sidney C. Smith, Jr, MD, FACC, FAHA, Past Chair 2006–2008 [§§][1]

Cynthia D. Adams, MSN, APRN-BC, FAHA[§§][1]

Nancy M

2012 ACCF/AHA/ACP/AATS/PCNA/SCAI/STS guideline for the diagnosis and management of patients with stable ischemic heart disease: executive summary: a report of the American College of Cardiology Foundation/American Heart Association task force on practice guidelines, and the American College of Physicians, American Association for Thoracic Surgery, Preventive Cardiovascular Nurses Association, Society for Cardiovascular Angiography and Interventions, and Society of Thoracic Surgeons.

Impairment of left ventricular function is the major predictor of mortality after acute myocardial infarction, but it is not known whether this is best described by ejection fraction or by end-systolic or end-diastolic volume. We measured volumes, ejection fractions, and severity of coronary arterial occlusions and stenoses in 605 male patients under 60 years of age at 1 to 2 months after a first (n = 443) or recurrent (n = 162) myocardial infarction and followed these patients for a mean of 78 months for survivors (range 15 to 165 months). There were 101 cardiac deaths, 71 (70%) of which were sudden (instantaneous or found dead). Multivariate analysis with log rank testing and the Cox proportional hazards model showed that end-systolic volume (chi 2 = 82.9) had greater predictive value for survival than end-diastolic volume (chi 2 = 59.0) or ejection fraction (chi 2 = 46.6), whereas stepwise analysis showed that once the relationship between survival and end-systolic volume had been fitted, there was no additional significant predictive information in either end-diastolic volume or ejection fraction. Severity of coronary occlusions and stenoses showed additional prediction of only borderline significance (p = .04 in one analysis), but continued cigarette smoking did remain an independent risk factor after stepwise analysis. For a subset of patients (n = 200) who had taken part in a randomized trial of coronary artery surgery after recovery from infarction, surgical "intention to treat" showed no predictive value.(ABSTRACT TRUNCATED AT 250 WORDS)

Left ventricular end-systolic volume as the major determinant of survival after recovery from myocardial infarction.

We studied the effects of cigarette smoking, sham smoking and smoking during adrenergic blockade in 10 subjects to determine whether smoking released the sympathetic neurotransmitter norepinephrine, as well as the adrenomedullary hormone epinephrine, and whether smoking-associated hemodynamic and metabolic changes were mediated through adrenergic mechanisms. Smoking-associated increments in mean (±S.E.M.) plasma norepinephrine (227±23 to 324±39 pg per milliliter, P<0.01) and epinephrine (44±4 to 113±27 pg per milliliter, P<0.05) were demonstrated. Smoking-associated increments in pulse rate, blood pressure, blood glycerol and blood lactate/pyruvate ratio were prevented by adrenergic blockade; increments in plasma growth hormone and cortisol were not. Since significant smoking-associated increments, in pulse rate, blood pressure and blood lactate/pyruvate ratio, preceded measurable increments in plasma catecholamine concentrations, but were adrenergically mediated, these changes should be attribut...

Norepinephrine and Epinephrine Release and Adrenergic Mediation of Smoking-Associated Hemodynamic and Metabolic Events

Significant advances in our knowledge about interventions to prevent cardiovascular disease (CVD) have occurred since publication of the first female-specific recommendations for preventive cardiology in 1999.1 Despite research-based gains in the treatment of CVD, it remains the leading killer of women in the United States and in most developed areas of the world.2–3 In the United States alone, more than one half million women die of CVD each year, exceeding the number of deaths in men and the next 7 causes of death in women combined. This translates into approximately 1 death every minute.2 Coronary heart disease (CHD) accounts for the majority of CVD deaths in women, disproportionately afflicts racial and ethnic minorities, and is a prime target for prevention.1–2 Because CHD is often fatal, and because nearly two thirds of women who die suddenly have no previously recognized symptoms, it is essential to prevent CHD.2 Other forms of atherosclerotic/thrombotic CVD, such as cerebrovascular disease and peripheral arterial disease, are critically important in women. Strategies known to reduce the burden of CHD may have substantial benefits for the prevention of noncoronary atherosclerosis, although they have been studied less extensively in some of these settings.

In the wake of the reports of the Women’s Health Initiative and the Heart and Estrogen/Progestin Replacement Study (HERS), which unexpectedly showed that combination hormone therapy was associated with adverse CVD effects, there is a heightened need to critically review and document strategies to prevent CVD in women.4–7 These studies underscore the importance of evidence-based practice for chronic disease prevention. Optimal translation and implementation of science to improve preventive care should include a rigorous process of evaluation and clear communication about the quantity and quality of evidence used to support clinical recommendations. Recently, there has been an increase in the …

Evidence-Based Guidelines for Cardiovascular Disease Prevention in Women

ContextAs more interventions become available for the treatment of coronary
heart disease (CHD), policy makers and health practitioners need to understand
the benefits of each intervention, to better determine where to focus resources.
This is particularly true when a patient with CHD quits smoking.ObjectiveTo conduct a systematic review to determine the magnitude of risk reduction
achieved by smoking cessation in patients with CHD.Data SourcesNine electronic databases were searched from start of database to April
2003, supplemented by cross-checking references, contact with experts, and
with large international cohort studies (identified by the Prospective Studies
Collaboration).Study SelectionProspective cohort studies of patients who were diagnosed with CHD were
included if they reported all-cause mortality and had at least 2 years of
follow-up. Smoking status had to be measured after CHD diagnosis to ascertain
quitting.Data ExtractionTwo reviewers independently assessed studies to determine eligibility,
quality assessment of studies, and results, and independently carried out
data extraction using a prepiloted, standardized form.Data SynthesisFrom the literature search, 665 publications were screened and 20 studies
were included. Results showed a 36% reduction in crude relative risk (RR)
of mortality for patients with CHD who quit compared with those who continued
smoking (RR, 0.64; 95% confidence interval [CI], 0.58-0.71). Results from
individual studies did not vary greatly despite many differences in patient
characteristics, such as age, sex, type of CHD, and the years in which studies
took place. Adjusted risk estimates did not differ substantially from crude
estimates. Many studies did not adequately address quality issues, such as
control of confounding, and misclassification of smoking status. However,
restriction to 6 higher-quality studies had little effect on the estimate
(RR, 0.71; 95% CI, 0.65-0.77). Few studies included large numbers of elderly
persons, women, ethnic minorities, or patients from developing countries.ConclusionsQuitting smoking is associated with a substantial reduction in risk
of all-cause mortality among patients with CHD. This risk reduction appears
to be consistent regardless of age, sex, index cardiac event, country, and
year of study commencement.

ThomasR Dawber

Papers

Death and coronary attacks in men after giving up cigarette smoking. A report from the Framingham study.