Risk Of Subsequent Myocardial Infarction Research Articles

The role of exercise training in peripheral arterial disease

Peripheral arterial disease (PAD) is currently a major health problem affecting 8-12 million Americans, 15-40% of whom will have intermittent claudication that can lead to substantial impairment in their ability to carry out normal daily activities as well as perform the recommended cardiovascular exercise. Supervised exercise training is an effective tool in the treatment of claudication and is currently a recommended first-line therapy for patients with this condition. In addition to improving pain-free walking distance and quality of life, supervised exercise training can improve many cardiovascular risk factors, possibly reducing the risk for subsequent myocardial infarction, stroke, and death. This paper will review the benefits of supervised exercise training in patients with PAD.

C-reactive protein, bezafibrate, and recurrent coronary events in patients with chronic coronary heart disease

Elevated C-reactive protein (CRP) levels are related to increased coronary risk in healthy subjects and in patients with acute coronary syndromes. The aims of the present study were to assess the following: (1) the association between CRP and subsequent coronary risk in patients with chronic coronary heart disease (CHD), (2) the effect of long-term bezafibrate treatment on CRP levels, and (3) to evaluate the consequences of change in CRP level over time on subsequent risk. Patients with chronic CHD (n = 3122) were recruited to a secondary prevention study that assessed the efficacy of bezafibrate versus placebo. C-reactive protein was measured in plasma samples collected at prerandomization and after 2 years of follow-up. Mean follow-up time was 6.2 years. Primary end point was fatal and nonfatal myocardial infarction and sudden cardiac death. Increased baseline CRP levels were associated with increased risk (hazard ratios [HRs] per unit of log-transformed CRP level change) of myocardial infarction (HR 1.17, 95% CI 1.03-1.33), the primary end point (HR 1.19, 95% CI 1.06-1.34), total death (HR 1.19, 95% CI 1.02-1.40) and cardiac death (HR 1.28, 95% CI 1.04-1.59). After 2 years, CRP levels increased by 3.0% (from a mean level of 3.44 mg/L) in the bezafibrate group and by 3.7% (from 3.49 mg/L) in the placebo group. C-reactive protein levels after 2 years were associated with increased subsequent cardiovascular risk. Baseline CRP and 2-year CRP levels were associated with subsequent risk of myocardial infarction and death in patients with chronic CHD. Bezafibrate did not reduce CRP levels as compared with placebo.

The impact of late career job loss on myocardial infarction and stroke: a 10 year follow up using the health and retirement survey

Background: Involuntary job loss is a major life event associated with social, economic, behavioural, and health outcomes, for which older workers are at elevated risk. Objective: To assess the 10...

Heart Disease and Dementia: A Population-based Study

There are conflicting reports on the possible positive association between coronary disease and dementia. The objectives of this study were to examine the association between coronary disease, as measured by myocardial infarction and cardiac death, and dementia in a population-based study. By use of the record-linkage system of the Rochester Epidemiology Project, 916 cases of dementia and 916 age (+/-1 year)- and sex-matched controls were identified in Rochester, Minnesota, between 1985 and 1994. From the same population, the authors identified all subjects who experienced a myocardial infarction (defined using standardized criteria) during the period 1979-1998. For myocardial infarction occurring prior to the index year of dementia, the authors used conditional logistic regression (case-control analysis), while for myocardial infarction and death occurring after the index year, they used competing risk survival analysis to account for informative censoring (cohort analysis). Before the index year, the odds ratio for myocardial infarction among cases with dementia compared with controls was 1.00 (95% confidence interval (CI): 0.62, 1.62; p = 1.00). After the index year, patients with dementia had a 46% decreased risk of subsequent myocardial infarction (hazard ratio = 0.54, 95% CI: 0.36, 0.82; p = 0.004) and an 18% decreased risk of cardiac death (hazard ratio = 0.82, 95% CI: 0.70, 0.95; p = 0.010). There was no evidence of a positive association between dementia and preceding myocardial infarction, while there was a decreased risk of myocardial infarction and cardiac death following dementia.

Involuntary job loss as a risk factor for subsequent myocardial infarction and stroke: findings from the Health and Retirement Survey.

The role of stress in the development of cardiovascular disease is well established. Previous research has demonstrated that involuntary job loss in the years immediately preceding retirement can be a stressful life event shown to produce adverse changes in physical and affective health. The objective of this study was to estimate the risk of myocardial infarction (MI) and stroke associated with involuntary job loss among workers nearing retirement in the United States. We used multivariable survival analysis to analyze data from the first four waves of the Health and Retirement Survey (HRS), a nationally representative sample of older individuals in the US. The analytic sample includes 457 workers who experienced job loss and a comparison group of 3,763 employed individuals. The results indicate that involuntary job loss is not associated with subsequent risk of MI (adjusted HR = 1.89; 95% CI = 0.91, 3.93); the risk of subsequent stroke associated with involuntary job loss is more than double (adjusted HR = 2.64; 95% CI = 1.01, 6.94). Our findings present new data to suggest that involuntary job loss should be considered as a plausible risk factor for subsequent cardiovascular and cerebrovascular illness among older workers.

Orthostatic hypotension and the risk of myocardial infarction in the home-dwelling elderly.

We investigated the prognostic significance of orthostatic hypotension on the risk of myocardial infarction (MI) amongst the elderly. Prospective population-based study. Home-dwelling population. Orthostatic testing was performed between 8 a.m. and 2 p.m., irrespective of having had meals, on 792 persons, representing 82% of all home-dwelling persons aged > or =70 years living in five municipalities around the city of Oulu. Occurrence of cases of MI were recorded during mean 3.58 (SD 1.09) years follow-up period, from national mortality statistics and local hospital discharge registers. Ninety cases of MI, of which 40 were fatal after initial hospitalization, occurred during the follow-up period. Orthostatic diastolic blood pressure (BP) drop 1 min after standing up was associated with subsequent MI, but systolic BP reactions had no predictive value. According to the Cox regression model, the strongest predictor of the occurrence of subsequent MI was found in regard to > or =8 mmHg drop in diastolic BP 1 min after standing up; adjusted for history of MI, diabetes mellitus, chest pain, use of calcium antagonist, beta-blocker, nitrate and diuretic medication, hazard ratio of MI being 2.00 (1.11-3.59). Orthostatic testing offers a novel means to assess the risk of MI amongst elderly persons. Diastolic BP drop immediately after standing up identifies elderly subjects at a high risk of subsequent MI.

Coagulation, inflammation and myocardial dysfunction in unstable coronary artery disease and the influence of glycoprotein IIb/IIIa inhibition and low molecular weight heparin

Patients with unstable coronary artery disease (CAD) have an increased risk of subsequent myocardial infarction and death. This study evaluated the safety and efficacy of treatment with glycoprotein IIb/IIIa inhibition in addition to aspirin, low molecular- weight heparin and its influence on coagulation and inflammation. Also, early and differentiated risk assessment utilising markers of inflammation, myocardial damage and dysfunction were evaluated.The Global Utilisation of Strategies To open Occluded arteries-IV (GUSTO-IV) trial randomised 7800 patients with unstable CAD to 24 or 48 hours infusion of abciximab or placebo in addition to routine treatment with aspirin and heparin or dalteparin. Baseline levels of creatinine, C-reactive protein (CRP), troponin T (TnT) and N-terminal pro-brain natriuretic peptide (NT-proBNP) were analysed. At selected sites, all patients received subcutaneous dalteparin (n=974), in stead of heparin infusion (n=6826). In a sub-population of dalteparin treated patients (n=404), serial measurements of markers of coagulation, fibrinolysis and inflammation were also performed. Addition of abciximab to dalteparin as the primary treatment of unstable CAD was not associated with any significant reduction in cardiac events but a doubled risk of bleedings. The combination of abciximab with dalteparin seemed as safe when used with heparin. Despite full dose dalteparin and aspirin there was a simultaneous activation of the inflammation, coagulation and fibrinolysis systems without any influence of the abciximab treatment. Elevated levels of CRP, TnT, and NT-proBNP and reduced creatinine clearance were independently related to short and long-term mortality. The best prediction of high and low risk was provided by a combination of NT-proBNP and creatinine clearance. Any detectable elevation of TnT and reduced creatinine clearance, but neither elevation of CRP nor NT-proBNP, were also independently associated to a raised risk of subsequent myocardial infarction.Abbreviations: Acute coronary syndrome (ACS), Brain natriuretic peptide (BNP), Coefficient of variance(CV), Coronary artery disease (CAD), Coronary artery bypass grafting (CABG), Creatine kinase-MB (CK-MB), C-reactive protein (CRP), Electrocardiogram (ECG), Glycoprotein IIb/IIIa (GPIIb/IIIa), Global Utilisation of Strategies To Open Occluded Arteries IV (GUSTO-IV), Interleukin-6(Il-6), Low-molecular weight heparin (LMWH), N-terminal pro-Brain natriuretic peptide (NT-proBNP),Myocardial infarction (MI), Percutaneous coronary intervention (PCI), Plasminogen activator(tPA), Plasminogen activator inhibitor (PAI-1), Soluble fibrin (SF), Thrombin-antithrombin complex(TAT), Troponin T (TnT), Unfractionated heparin (UFH).

Troponin and C-reactive protein have different relations to subsequent mortality and myocardial infarction after acute coronary syndrome: A GUSTO-IV substudy

ObjectivesWe sought to evaluate C-reactive protein (CRP) and troponin T (TnT) as predictors of risk of the individual end points of mortality and myocardial infarction (MI) in a large cohort of patients with acute coronary syndrome (ACS). BackgroundBoth CRP and TnT predict risk of future coronary events in patients with ACS. However, the relationships between the levels of the markers and the individual end points are still unclear. MethodsBaseline levels of CRP and TnT were determined in 7,108 patients with ACS not undergoing early revascularization in the Global Use of Strategies To Open occluded arteries trial IV (GUSTO-IV) trial and related to outcome at 30 days. ResultsQuartiles of TnT related to 30-day mortality, which was 1.1%, 3.7%, 3.7%, and 7.4% (p < 0.001) and to the rate of MI: 2.5%, 6.7%, 7.2%, and 5.6% (p < 0.001). Quartiles of CRP also related to 30-day mortality, which was 2.0%, 3.3%, 3.9%, and 6.3% (p < 0.001), whereas there was no relationship to the 30-day rate of MI: 5.6%, 4.7%, 5.2%, and 5.9% (p = 0.48). On multivariable analysis, both TnT and CRP were independent predictors of mortality, but only TnT was a predictor of MI. The combination of CRP and TnT provides an even better risk stratification of mortality, with 0.3% and 9.1% death rates, respectively, when both markers are in the bottom versus top quartiles. ConclusionsIn ACS, baseline levels of TnT and CRP are independently related to 30-day mortality. Any detectable elevation of TnT, but not of CRP, is also associated with an increased risk of subsequent MI. Regarding mortality, the combination of both markers provides a better risk stratification than either one alone.

C-reactive protein, Helicobacter pylori, Chlamydia pneumoniae, cytomegalovirus and risk for myocardial infarction.

C-reactive protein (CRP), Chlamydia pneumonia, Helicobacter pylori, and cytomegalovirus (CMV) have each been associated with atherosclerosis. We assessed how infection and CRP related to risk for subsequent myocardial infarction (MI). Using a nested case-control design, we assessed how these factors independently and jointly affected risk for myocardial infarction (MI). Cases of first MI (N = 121) were identified from among participants in a multiphasic health check-up cohort. Controls without MI (N = 204) were matched to cases by gender, age, race, and date of serum collection. Sera collected at enrollment were tested for antibodies to infection and for CRP. In multivariate analysis (mean follow-up of 5.1 years), CRP was associated with MI only in subjects older than 51 years (p = 0.004). Although H. pylori infection increased risk for MI, this association was modest (OR = 1.90, 95% CI = 0.97-3.71) and was not evident in non-smokers or when adjusted for education. No association between C. pneumoniae or cytomegalovirus and MI was observed, nor was the association between CRP and MI explained by these infections. Elevated CRP is a risk factor for subsequent MI in older individuals. The relationship between Hp and MI may be due to confounding or co-linearity with socioeconomic status.

Magnetic resonance imaging assessment of cardiac function.

Measurements of left ventricular function at rest and during stress are useful for identifying myocardial ischemia, injury, and the risk of subsequent myocardial infarction. Without ionizing radiation or intravascular contrast administration, magnetic resonance imaging techniques can be used to acquire precise measurements of left ventricular function. This relatively new development may enhance a physician's ability to provide care to patients with cardiovascular disease.

Multiple Infections and Subsequent Cardiovascular Events in the Heart Outcomes Prevention Evaluation (HOPE) Study

Limited prospective epidemiological data are available on the relation between exposure to Chlamydia pneumoniae, Helicobacter pylori, cytomegalovirus (CMV), and hepatitis A virus (HAV), individually or as a total pathogen score, and human cardiovascular (CV) disease. We analyzed enrollment sera from 3168 Canadian patients in the Heart Outcomes Prevention Evaluation (HOPE) study for antibodies to C pneumoniae, H pylori, CMV, and HAV and measured the relation between serostatus and 494 adjudicated trial outcomes of myocardial infarction, stroke, or CV death over 4.5 years of follow-up. CV events were associated with CMV serostatus (covariate-adjusted hazard ratio [HR], 1.24; 95% CI, 1.01, 1.53). Neither C pneumoniae IgG (adjusted HR, 0.87; 95% CI, 0.68, 1.10), C pneumonia IgA (adjusted HR, 1.10; 95% CI, 0.90, 1.34), H pylori IgG (HR, 0.99; 95% CI, 0.82, 1.19), nor HAV IgG (HR, 1.01; 95% CI, 0.83, 1.24) predicted CV events. Total pathogen score was associated with CV events (adjusted HR for 4 versus 1 or 0=1.41; 95% CI, 1.02, 1.96). Exposure to CMV but not to C pneumoniae, H pylori, or HAV was associated with a slight excess risk of subsequent myocardial infarction, stroke, or CV death in HOPE study patients, and total pathogen score based on these infections predicted a small increased hazard of CV events.

Pharmacologic therapy for peripheral arterial disease and claudication.

Peripheral arterial disease (PAD) is a common manifestation of systemic atherosclerosis that is associated with a high risk of cardiovascular mortality and significant limitation in function because of limb ischemia. Patients with PAD should be considered to have significant coronary and cerebral arterial disease that requires aggressive risk factor management, including the prescription of antiplatelet drugs, to lower the subsequent risk of myocardial infarction, stroke, and death. In the population with PAD, level 1 and level 2 evidence supports the use of statin drugs for lipid management, angiotensin-converting enzyme-1 inhibitors for blood pressure control, and aspirin or clopidogrel as antiplatelet agents. Once this is accomplished, the severity of limb symptoms should be assessed, and a structured exercise program or the selected use of drugs such as cilostazol to treat claudication should be prescribed. In patients primarily considered for surgical treatment, antiplatelet and anticoagulant drug therapy can be used as a means of promoting graft patency, and beta-adrenergic blockers can be used as a means of reducing the perioperative risks associated with vascular surgery.

Platelet glycoprotein Ib alpha receptor polymorphisms and recurrent ischaemic events in acute coronary syndrome patients.

To examine the relationship between polymorphisms in the platelet receptor glycoprotein (GP) Ib(alpha) and recurrent ischaemic events, and assess their impact on response to anti-platelet treatment. 1014 patients presenting with unstable coronary syndrome were recruited from the OPUS-TIMI 16 clinical trial of the platelet GPIIb/IIIa antagonist, orbofiban. The subjects were genotyped for two polymorphisms in the gene for GPIb(alpha). These were a T-5C polymorphism in the 5' untranslated Kozak region of the GPIb(alpha) gene, and the variable number of tandem repeats (VNTR) in the macroglycopeptide region.165 patients had events (recurrent ischaemia, urgent revascularisation, myocardial infarction (MI), stroke and death). There was no effect of the number of -5C alleles on composite endpoint frequency among Caucasian subjects (test for trend, p = 0.47). However, MI risk increased with the number of -5C alleles carried, with MI occurring in 2.3% of patients with the -5T/-5T genotype, 5.0% of -5T/-5C, and 16.7% of -5C/-5C (p < 0.01). The effect of treatment on MI outcome was not significantly modified by genotype (test for interaction, p = 0.10). The overall risk of bleeding was not strongly influenced by either the -5C or the VNTR polymorphisms. In an unstable coronary syndrome population the T-5C polymorphism in GPIb(alpha) influences risk of subsequent MI.

Self-Selected Posttrial Aspirin Use and Subsequent Cardiovascular Disease and Mortality in the Physicians' Health Study

The randomized aspirin component of the Physicians' Health Study (PHS) was terminated early, after 5 years, primarily because of the emergence of a statistically extreme (P<.00001) 44% reduction of first myocardial infarction (MI) among those assigned to aspirin. As a result, there were insufficient numbers of strokes or cardiovascular disease (CVD)-related deaths to evaluate these end points definitively. Data on self-selected aspirin use were collected until the beta carotene component ended as scheduled after 12 years. Posttrial use of aspirin was assessed at the 7-year follow-up among 18 496 participants with no previous reported CVD. Randomized and posttrial observational results in the PHS were compared, and differences between those self-selecting aspirin and those not were examined. At 7 years, 59.5% of participants without CVD reported self-selected aspirin use for at least 180 d/y, and 20.8% for 0 to 13 d/y. Use was significantly associated with family history of MI, hypertension, elevated cholesterol levels, body mass index, alcohol consumption, exercise, and use of vitamin E supplements. In multivariate analyses, self-selected aspirin use for at least 180 vs 0 to 13 d/y was associated with lower risk for subsequent MI (relative risk [RR], 0.72; 95% confidence interval [CI], 0.55-0.95), no relation with stroke (RR, 1.02; 95% CI, 0.74-1.39), and significant reductions in CVD-related (RR, 0.65; CI, 0.47-0.89) and total mortality (RR, 0.64; CI, 0.54-0.77). These associations between self-selected aspirin use and CVD risk factors increase the likelihood of residual confounding and emphasize the need for large-scale randomized trials, such as the ongoing Women's Health Study, to detect reliably the most plausible small to moderate effects of aspirin in the primary prevention of stroke and CVD-related death.

PI A1/A2 polymorphism of platelet glycoprotein IIIa and risks of myocardial infarction, stroke, and venous thrombosis

The gene encoding the platelet glycoprotein IIIa receptor (GPIIIa), shows polymorphism (PIA1/A2). In a previous study, men with acute coronary ischaemia were more likely than controls to carry the PIA2 allele. This receptor has an important role in acute thrombus formation; these findings therefore raise the possibility of inherited platelet risk factors for both arterial and venous thrombosis. We investigated whether the PIA2 allele is associated with myocardial infarction, stroke, and venous thrombosis in a large prospective cohort of men in the USA. 14916 initially healthy men participating in the Physicians Health Study provided baseline blood specimens for DNA analysis and were followed prospectively for a mean of 8.6 years. 374 men had a first myocardial infarction, 209 stroke, and 121 venous thrombosis during follow-up (704 cases). Distribution of the PIA1/A2 polymorphism was investigated by a PCR based on restriction-fragment length polymorphism in these men and in a sample of 704 matched study participants who remained free of thrombosis during follow-up (controls). The frequency of the PIA2 allele was similar to the control frequency (14.8%) among men who had myocardial infarction (13.5%, p = 0.4), stroke (13.4%, p = 0.5), or venous thrombosis (14.5%, p = 0.9). The relative risk of any vascular event among men homozygous or heterozygous for PIA2 compared with men homozygous for PIA1 was 0.96 (95% CI 0.8-1.2). We found no evidence of association between the PIA2 allele and myocardial infarction (relative risk 0.93 [95 0.7-1.2]), stroke (0.93 [0.7-1.3]), or venous thrombosis (1.07 [0.7-1.6]). There was no evidence of association in subgroup analyses by age, smoking status, and presence of family history of premature coronary disease, hypercholesterolaemia, hypertension, or diabetes. Aspirin use had no effect on these findings. In a large cohort of apparently healthy men, carriage of the GPIIIa PIA2 allele was not associated with any increase in subsequent risk of myocardial infarction, stroke, or venous thrombosis.

Angiographic correlates of graft patency and relationship to clinical outcomes

Retained graft patency after revascularization lowers risk of subsequent myocardial infarction or death. Patients who have surgical rather than medical therapy are far less likely to die of a subsequent nonperioperative infarction. Both myocardial infarction size and lethality are modified by prior coronary artery bypass grafting. The procedure risk for either death or nonfatal infarction remains higher in coronary artery bypass grafting than in angioplasty, but among patients who survive for 30 days, subsequent risk is only two-thirds that of patients who had angioplasty. Better graft patency rates are associated with the use of an internal thoracic artery rather than a saphenous vein, larger size of the recipient coronary artery, and better blood flow through the grafts. Aspirin therapy clearly decreases the occlusion rate per distal anastomosis, but aprotinin therapy appears to have little or no effect on graft patency. Numerous other factors can influence graft patency. Prominent among the factors increasing risk for requirement of a reoperation are nonuse of an internal thoracic artery, incomplete revascularization, and continued cigarette smoking.

Relation of C-reactive protein and coronary heart disease in the MRFIT nested case-control study. Multiple Risk Factor Intervention Trial.

The authors measured the relation between C-reactive protein, alpha 1 acid glycoprotein and albumin, an acute phase protein, and subsequent risk of myocardial infarction and coronary heart disease death in a nested case-control study among the Multiple Risk Factor Intervention Trial (MRFIT) participants. There were 98 myocardial infarction cases, 148 coronary heart disease deaths, and 491 controls. The cases and controls were followed for up to 17 years for deaths and 6-7 years for myocardial infarction cases and controls. There was a significant association between available distribution of C-reactive protein and subsequent coronary heart disease mortality. For smokers at baseline, the risk of coronary heart disease deaths in quartile 4 of C-reactive protein as compared with quartile 1 was 4.3 (95% confidence interval 1.74-10.8). The association persisted when adjusted for characteristics related to smoking and smoking cessation during the trial and to pulmonary function. There was no relation between alpha 1 acid glycoprotein and either myocardial infarction or coronary heart disease death. Albumin was inversely related to coronary heart disease death only for deaths that occurred between 7 and 13 years after baseline, consistent with previous MRFIT analyses. This is the first prospective study in "healthy but high risk individuals" to document the relation between C-reactive protein and coronary heart disease mortality.

Randomised controlled trial of vitamin E in patients with coronary disease: Cambridge Heart Antioxidant Study (CHAOS)

Summary Background Vitamin E (α-tocopherol) is thought to have a role in prevention of atherosclerosis, through inhibition of oxidation of low-density lipoprotein. Some epidemiological studies have shown an association between high dietary intake or high serum concentrations of α-tocopherol and lower rates of ischaemic heart disease. We tested the hypothesis that treatment with a high dose of α-tocopherol would reduce subsequent risk of myocardial infarction (MI) and cardiovascular death in patients with established ischaemic heart disease. Methods In this double-blind, placebo-controlled study with stratified randomisation, 2002 patients with angiographically proven coronary atherosclerosis were enrolled and followed up for a median of 510 days (range 3-981). 1035 patients were assigned α-tocopherol (capsules containing 800 IU daily for first 546 patients; 400 IU daily for remainder); 967 received identical placebo capsules. The primary endpoints were a combination of cardiovascular death and non-fatal MI as well as non-fatal Ml alone. Findings Plasma α-tocopherol concentrations (measured in subsets of patients) rose in the actively treated group (from baseline mean 34·2 μmol/L to 51·1 μmol/L with 400 IU daily and 64·5 μmol/L with 800 IU daily) but did not change in the placebo group. α-tocopherol treatment significantly reduced the risk of the primary trial endpoint of cardiovascular death and non-fatal Ml (41 vs 64 events; relative risk 0·53 [95% Cl 0·34-0·83; p=0·005). The beneficial effects on this composite endpoint were due to a significant reduction in the risk of non-fatal Ml (14 vs 41; 0·23 [0·11-0·47]; p=0·005); however, there was a non-significant excess of cardiovascular deaths in the α-tocopherol group (27 vs 23; 1·18 [0·62-2·27]; p=0·61). All-cause mortality was 36 of 1035 α-tocopherol-treated patients and 27 of 967 placebo recipients. Interpretation We conclude that in patients with angiographically proven symptomatic coronary atherosclerosis, α-tocopherol treatment substantially reduces the rate of non-fatal MI, with beneficial effects apparent after 1 year of treatment. The effect of α-tocopherol treatment on cardiovascular deaths requires further study.

Identifying Patient Risk: The Basis for Rational Discharge Planning After Acute Myocardial Infarction.

Variations in the management of patients with chest pain and acute myocardial infarction (MI) can significantly affect hospital length of stay and cost. Risk stratification of such patients, combined with data about effective therapies, provides the basis for developing rational guidelines for patient care that can improve efficiency while maintaining quality of care. Such standardized management approaches are often referred to as pathways or CareMaps. To be most effective in guiding hospital course and early discharge planning, risk stratification strategies must be applied early in a patient's course with continuous updating. The process of identifying risk in a patient with acute chest pain occurs in two segments: assessing the risk of acute MI at presentation, and subsequently assessing the morbidity and mortality risk of patients diagnosed with acute MI. Identification of patient risk at presentation has been the object of intense investigation. The history, physical exam, initial electrocardiogram, and cardiac enzymes are the mainstays of the process, but because of inherent weaknesses in this approach (>25% of acute MIs missed initial screening), several risk stratification models have been developed. To date these models have not been widely employed, however. Very sensitive early cardiac markers, such as troponin T, and the use of diagnostic echocardiography or cardiolite perfusion imaging during pain are also being investigated. Chest pain observation units are an alternate strategy and have obviated the need to admit many low- to moderate-risk chest pain patients. In these protocol-driven units, continuous physiologic monitoring and serial cardiac enzymes and electrocardiography over a 9-12 hour period refine the risk assessment. For the majority who "rule out," the risk of subsequent MI or death is very low. Cost savings due to reduced length of stay and more efficient resource utilization are 63-76% compared with conventional word or cardiac care unit management. For patients with acute MI, baseline characteristics, complications, and laboratory and diagnostic testing help define the risk of morbidity and mortality and guide management through the immediate post-MI phase and long term. Many models incorporating these features have been proposed for risk stratification after acute MI, and they have implications for both timing of discharge and necessary diagnostic testing. Savings by employing risk stratification to guide hospital course and discharge planning could be 30-44% in some patient groups. In conclusion, risk stratification models can facilitate early discharge planning, potentially reducing hospital stay, improving resource utilization, and reducing costs.

901-79 Borderline Isolated Systolic Hypertension and Subsequent Risk of Cardiovascular Disease

Guidelines are unclear about treatment of borderline isolated systolic hypertension, defined as both systolic BP 140-159 mmHg and diastolic BP &lt; 90 mmHg. We investigated the association between borderline isolated systolic hypertension and subsequent risk of myocardial infarction (Ml), stroke, cardiovascular death, and the combined endpoint of important cardiovascular events (nonfatal MI, nonfatal stroke or cardiovascular death) among 22,071 men age 40-84 years followed prospectively for an average of 10.7 years in the Physician's Health Study. Baseline BP and cardiovascular risk factors were available from completed questionnaires on 16,678 men among whom 960 subsequently had an incident important cardiovascular event. In proportional hazards models adjusting for other cardiovascular risk factors, the relative risks were calculated for those with borderline isolated systolic hypertension relative to those with both systolic BP &lt; 140 mmHg and diastolic BP &lt; 90 mmHg. These relative risks were 1.05 (95% confidence interval Cl 0.80 to 1.36) for Ml, 1.68 (95% Cl 1.24 to 2.26) for stroke, 1.61 (95% Cl 1.19 to 2.18) for cardiovascular death, and 1.32 (95% Cl 1.11 to 1.58) for the combined endpoint of important cardiovascular events. These associations were not altered by an analysis excluding participants who reported baseline treatment for hypertension. Borderline isolated systolic hypertension is associated with a significantly increased risk of subsequent important cardiovascular events.