Ira S. Ockene
University of Massachusetts Medical School
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Circulation | 2002
Thomas A. Pearson; Steven N. Blair; Stephen R. Daniels; Robert H. Eckel; Joan M. Fair; Stephen P. Fortmann; Barry A. Franklin; Larry B. Goldstein; Philip Greenland; Scott M. Grundy; Yuling Hong; Nancy Houston Miller; Ronald M. Lauer; Ira S. Ockene; Ralph L. Sacco; James F. Sallis; Sidney C. Smith; Neil J. Stone; Kathryn A. Taubert
The initial Guide to the Primary Prevention of Cardiovascular Diseases was published in 1997 as an aid to healthcare professionals and their patients without established coronary artery disease or other atherosclerotic diseases.1 It was intended to complement the American Heart Association (AHA)/American College of Cardiology (ACC) Guidelines for Preventing Heart Attack and Death in Patients with Atherosclerotic Cardiovascular Disease (updated2) and to provide the healthcare professional with a comprehensive approach to patients across a wide spectrum of risk. The imperative to prevent the first episode of coronary disease or stroke or the development of aortic aneurysm and peripheral arterial disease remains as strong as ever because of the still-high rate of first events that are fatal or disabling or require expensive intensive medical care. The evidence that most cardiovascular disease is preventable continues to grow. Results of long-term prospective studies consistently identify persons with low levels of risk factors as having lifelong low levels of heart disease and stroke.3,4⇓ Moreover, these low levels of risk factors are related to healthy lifestyles. Data from the Nurses Health Study,5 for example, suggest that in women, maintaining a desirable body weight, eating a healthy diet, exercising regularly, not smoking, and consuming a moderate amount of alcohol could account for an 84% reduction in risk, yet only 3% of the women studied were in that category. Clearly, the majority of the causes of cardiovascular disease are known and modifiable. This 2002 update of the Guide acknowledges a number of advances in the field of primary prevention since 1997. Research continues to refine the recommendations on detection and management of established risk factors, including evidence against the safety and efficacy of interventions once thought promising (eg, antioxidant vitamins).6 This, in turn, has …
Journal of the American College of Cardiology | 1988
A. Koneti Rao; Craig M. Pratt; Berke A; Allan Jaffe; Ira S. Ockene; Theodore Schreiber; William R. Bell; Genell L. Knatterud; Thomas L. Robertson; Michael L. Terrin
Abstract Two hundred ninety patients with acute myocardial infarction were treated according to random assignment with an intravenous infusion of either 80 mg of recombinant tissue plasminogen activator (rt-PA) over 3 h or 1.5 million units of Streptokinase over 1 h. Patients received an intravenous bolus of heparin (5,000 U [USP]) before pretreatment coronary angiography and a continuous infusion (1,000 U/h) starting 3 h later. The frequency of major and minor hemorrhagic events (33% rt-PA, 31% Streptokinase) and associated transfusions (22% rt-PA, 20% streptokinase) were comparable in both groups. More than 70% of bleeding episodes in each group occurred at catheterization or vascular puncture sites. Precipitable fibrinogen levels, measured in plasma samples collected in the presence of a protease inhibitor (aprotinin), declined in rt-PA and streptokinase groups by averages of 26 and 57% at 3 h and by 33 and 58% at 5 h, respectively (rt-PA versus streptokinase, p Thus, in the doses administered, rt-PA induces systemic fibrinogenolysis that is substantially less intense than that induced by streptokinase. The high frequency of bleeding encountered is retated to the protocol used, including vigorous anticoagulation, arterial punctures and thrombolytic therapy. These findings emphasize the need for avoidance of invasive procedures and for meticulous care in the selection and management of patients subjected to thrombolytic therapy.
Circulation | 2001
Sidney C. Smith; Steven N. Blair; Robert O. Bonow; Lawrence M. Brass; Manuel D. Cerqueira; Kathleen Dracup; Valentin Fuster; Antonio M. Gotto; Scott M. Grundy; Nancy Houston Miller; Alice K. Jacobs; Daniel Jones; Ronald M. Krauss; Lori Mosca; Ira S. Ockene; Richard C. Pasternak; Thomas A. Pearson; Marc A. Pfeffer; Rodman D. Starke; Kathryn A. Taubert
Since the original publication (in 1995) of the American Heart Association (AHA) consensus statement on secondary prevention, which was endorsed by the American College of Cardiology (ACC), important evidence from clinical trials has emerged that further supports the merits of aggressive risk reduction therapies for patients with atherosclerotic cardiovascular disease. As noted in that statement, aggressive risk factor management clearly improves patient survival, reduces recurrent events and the need for interventional procedures, and improves the quality of life for these patients. The compelling evidence from recent clinical trials was the impetus …
Circulation | 1998
Scott M. Grundy; Gary J. Balady; Michael H. Criqui; Gerald F. Fletcher; Philip Greenland; Loren F. Hiratzka; Nancy Houston-Miller; Penny M. Kris-Etherton; Harlan M. Krumholz; John C. LaRosa; Ira S. Ockene; Thomas A. Pearson; James Reed; Reginald L. Washington; Sidney C. Smith
The Framingham Heart Study has contributed importantly to understanding of the causes of coronary heart disease (CHD), stroke, and other cardiovascular diseases. Framingham research has helped define the quantitative and additive nature of these causes or, as they are now called, “cardiovascular risk factors.”1 The National Cholesterol Education Program (NCEP)2 3 has made extensive use of Framingham data in developing its strategy for preventing CHD by controlling high cholesterol levels. The NCEP guidelines2 3 adjust the intensity of cholesterol-lowering therapy with absolute risk as determined by summation of risk factors. The National High Blood Pressure Education Program (NHBPEP) has set forth a parallel approach for blood pressure control. In contrast to the NCEP,2 however, earlier NHBPEP reports issued through the Joint National Committee4 did not match the intensity of therapy to absolute risk for CHD. “Normalization” of blood pressure is the essential goal of therapy regardless of risk status. Blood pressure–lowering therapy is carried out as much for prevention of stroke and other cardiovascular complications as for reduction of CHD risk. Nonetheless, risk assessment could be important for making decisions about type and intensity of therapy for hypertension. Thus, the most recent Joint National Committee report5 gives more attention to risk stratification for adjustment of therapy for hypertension. Although Framingham data have already been influential in the development of national guidelines for risk factor management, the opportunity may exist for both cholesterol and blood pressure programs to draw more extensively from Framingham results when formulating improved risk assessment guidelines and recommending more specific strategies for risk factor modification. The American Heart Association has previously used Framingham risk factor data to prepare charts for estimating CHD risk. Framingham investigators of the National Heart, Lung, and Blood Institute prepared the original charts and have now revised …
Circulation | 1997
Nancy Houston Miller; Martha N. Hill; Thomas E. Kottke; Ira S. Ockene
Despite the universally accepted importance of compliance, strategies known for more than two decades to be effective are not routinely incorporated into clinical practice. For the benefits of primary and secondary prevention to be realized in diverse population groups and settings, emphasis must be placed on implementing strategies at the patient, provider, and organization levels. Current knowledge of compliance strategies, if integrated into a multilevel approach, offers enormous promise for decreasing risk and improving patient outcomes.
Circulation | 1997
Ira S. Ockene; Nancy Houston Miller
As many as 30% of all coronary heart disease (CHD) deaths in the United States each year are attributable to cigarette smoking, with the risk being strongly dose-related.1 2 Smoking also nearly doubles the risk of ischemic stroke.3 Smoking acts synergistically with other risk factors, substantially increasing the risk of CHD.4 Smokers are also at increased risk for peripheral vascular disease, cancer, chronic lung disease, and many other chronic diseases. Cigarette smoking is the single most alterable risk factor contributing to premature morbidity and mortality in the United States, accounting for approximately 430 000 deaths annually.5 Numerous prospective investigations have demonstrated a substantial decrease in CHD mortality for former smokers compared with continuing smokers.6 This diminution in risk occurs relatively soon after cessation of smoking, and increasing intervals since the last cigarette smoked are associated with progressively lower mortality rates from CHD.7 Similar rapid decreases in risk with smoking cessation are also seen for ischemic stroke.8 9 Benefits from quitting are seen in former smokers even after many years of heavy smoking.2 Investigations also have demonstrated benefits from cessation for smokers who have already developed smoking-related diseases or symptoms. Persons with diagnosed CHD experience as much as a 50% reduction in risk of reinfarction, sudden cardiac death, and total mortality if they quit smoking after the initial infarction.10 11 Furthermore, the patient who has recently developed a clinical illness is very motivated to change, and several studies have shown that intervention in this “teachable moment” can be very effective. Thus, the provision of smoking cessation advice is associated with a 50% long-term (more than 1 year) smoking cessation rate in patients who have been hospitalized with a coronary event, and even modest telephone-based counseling can increase this percentage to ≥70% in …
The New England Journal of Medicine | 1980
Ira S. Ockene; Marilyn Shay; Joseph S. Alpert; Bonnie H. Weiner; James E. Dalen
Approximately 10 per cent of patients referred for coronary arteriography because of chest pain have angiographically normal coronary arteries and no other heart disease. We examined the functional status of 57 patients who had undergone catheterization (23 men and 34 women), all of whom were told that their hearts were normal, that their pain was noncardiac, and that no limitation on activity was necessary. At a mean follow-up time of 16 +/- 7.7 months, 27 of the 57 patients (47 per cent) still described their activity as limited by chest pain (before catheterization, 42 of 57 or 74 per cent); 29 of 57 (51 per cent) were unable to work (before catheterization, 36 of 57 or 63 per cent); and 25 of 57 (44 per cent) still believed that they had heart disease (before catheterization, 45 of 57 or 79 per cent). Use of medical facilities was significantly reduced after catheterization (P < 0.001). At follow-up the physician was more likely than the patient to believe that the symptoms had improved. We conclude that many of these patients remain limited in activity and may benefit from further efforts at comunication and rehabilitation.
JAMA Internal Medicine | 2012
Annie L. Culver; Ira S. Ockene; Raji Balasubramanian; Barbara C. Olendzki; Deidre M. Sepavich; Jean Wactawski-Wende; JoAnn E. Manson; Yongxia Qiao; Simin Liu; Philip A. Merriam; Catherine Rahilly-Tierny; Fridtjof Thomas; Judith K. Ockene; J. David Curb; Yunsheng Ma
BACKGROUND This study investigates whether the incidence of new-onset diabetes mellitus (DM) is associated with statin use among postmenopausal women participating in the Womens Health Initiative (WHI). METHODS The WHI recruited 161,808 postmenopausal women aged 50 to 79 years at 40 clinical centers across the United States from 1993 to 1998 with ongoing follow-up. The current analysis includes data through 2005. Statin use was captured at enrollment and year 3. Incident DM status was determined annually from enrollment. Cox proportional hazards models were used to estimate the risk of DM by statin use, with adjustments for propensity score and other potential confounding factors. Subgroup analyses by race/ethnicity, obesity status, and age group were conducted to uncover effect modification. RESULTS This investigation included 153,840 women without DM and no missing data at baseline. At baseline, 7.04% reported taking statin medication. There were 10,242 incident cases of self-reported DM over 1,004,466 person-years of follow-up. Statin use at baseline was associated with an increased risk of DM (hazard ratio [HR], 1.71; 95% CI, 1.61-1.83). This association remained after adjusting for other potential confounders (multivariate-adjusted HR, 1.48; 95% CI, 1.38-1.59) and was observed for all types of statin medications. Subset analyses evaluating the association of self-reported DM with longitudinal measures of statin use in 125,575 women confirmed these findings. CONCLUSIONS Statin medication use in postmenopausal women is associated with an increased risk for DM. This may be a medication class effect. Further study by statin type and dose may reveal varying risk levels for new-onset DM in this population.
Circulation | 2002
Mark A. Williams; Jerome L. Fleg; Philip A. Ades; Bernard R. Chaitman; Nancy Houston Miller; Syed M. Mohiuddin; Ira S. Ockene; C. Barr Taylor; Nanette K. Wenger
The overall aging of the American population and improving survival of patients with coronary heart disease (CHD) has created a large population of older adults (≥65 years of age) eligible for secondary prevention. The prevalence of chronic ischemic heart disease in men and women ≥65 years of age in the United States in 1995 was 83 per 1000 men and 90 per 1000 women. Among those ≥75 years of age, the prevalences were 217 per 1000 for men and 129 per 1000 for women.1 Increasing evidence has accumulated over the past 2 decades that elderly individuals with CHD can benefit greatly from exercise training and other aspects of secondary prevention.2 Traditionally, components of secondary prevention programming (including exercise; smoking cessation; management of dyslipidemia, hypertension, diabetes, and weight; and interventions directed at depression, social isolation, return to work, and other psychosocial issues) have been provided by the clinician in the office setting or through cardiac rehabilitation programs. Cardiac rehabilitation programs are particularly well suited to the provision of secondary prevention services, but unfortunately, many older patients who would derive benefit from these interventions do not participate because of lack of referral or a variety of societal and other barriers.3 It is the purpose of this Scientific Statement to provide an update on the benefits of specific secondary prevention risk factor interventions in this age group and, where possible, to delineate benefits in the older elderly (≥75 years of age). An increased awareness on the part of physicians, nurses, third-party payers, and patients and their families of the benefits of secondary prevention programs to older adults will provide a basis for referral and aid in the implementation of such programming. The clinical manifestations of CHD in older patients represent the effects of the disease superimposed on the physiological effects …
The New England Journal of Medicine | 1986
Bonnie H. Weiner; Ira S. Ockene; Peter H. Levine; Henri F. Cuenoud; Marc Fisher; Brian F. Johnson; A.S. Daoud; J. Jarmolych; David W. Hosmer; Mark H. Johnson
We studied the effect of cod-liver oil on the development and progression of coronary artery disease in swine subjected to coronary balloon abrasion and fed an atherogenic diet for eight months. Sections from serial 3-mm segments of the coronary arteries were analyzed morphometrically in 7 pigs given a cod-liver-oil supplement and 11 control animals not given the supplement. Significantly less disease was seen in the sections from the animals fed cod-liver oil. The mean lesion area per vessel, mean luminal encroachment per vessel, and mean maximal luminal encroachment per vessel were reduced in animals fed cod-liver oil, as compared with controls, (P = 0.05, P = 0.016, and P = 0.011, respectively). Both groups of animals had severe hyperlipidemia throughout the study. Differences in the extent of coronary atherosclerosis were not related to differences in plasma lipid levels. Platelet arachidonate was markedly reduced, platelet eicosapentaenoic acid was increased, and serum thromboxane was decreased in the oil-fed group as compared with the control group. We conclude that in our animal mode, dietary cod-liver oil retarded the development of coronary artery disease, possibly through changes in prostaglandin metabolism.