Risk Of Recurrent Coronary Events Research Articles

Influenza vaccination is not associated with a reduction in the risk of recurrent coronary events.

Acute respiratory infections, including influenza, have been suggested as possible precipitants of acute cardiac events. To evaluate whether influenza vaccination prevents recurrent coronary events, the authors conducted a population-based inception cohort study of 1,378 Group Health Cooperative enrollees who survived a first myocardial infarction in 1992 through 1996. Recurrent coronary events, influenza vaccinations, and other covariates were identified by chart review and from administrative data systems. A Cox proportional hazards model was used to evaluate the association of receipt of each year's influenza vaccine with subsequent risk of recurrent myocardial infarction and death from atherosclerotic cardiovascular disease. A total of 127 recurrent coronary events were identified during the median 2.3-year follow-up period. Influenza vaccination was not associated with risk of recurrent coronary events during the corresponding period of November through October (adjusted hazard ratio (HR) = 1.18, 95% confidence interval (CI): 0.79, 1.75) or during the corresponding periods of expected influenza activity (November through April) (HR = 1.06, 95% CI: 0.63, 1.78) or inactivity (May through October) (HR = 1.34, 95% CI: 0.76, 2.36). These results suggest that the benefit of influenza vaccine for older adults does not extend to protection against recurrent coronary events.

Smoking Status and Risk for Recurrent Coronary Events after Myocardial Infarction

Questions remain about the importance of smoking and smoking cessation after incident myocardial infarction. To assess the association between smoking status and risk for recurrent coronary events. Retrospective, population-based, inception cohort study. Health maintenance organization from 1986 to 1996. 2619 persons who survived to hospital discharge after a first myocardial infarction. Relative risk (RR), assessed by using Cox proportional hazards regression analysis, for recurrent coronary events in nonsmokers (persons with no history of smoking), former smokers (persons who had stopped smoking before infarction), quitters (persons who stopped smoking after infarction), and active smokers (persons who continued smoking after infarction). At the time of incident infarction, 33.6% of patients were nonsmokers, 35.5% were former smokers, and 30.9% were active smokers. Of the 808 persons who were active smokers at the time of incident infarction, 449 quit smoking during hospitalization or after discharge. With nonsmokers as the reference group, the multivariable RR for recurrent coronary events (n = 433) was 1.17 (95% CI, 0.93 to 1.43) for former smokers and 1.51 (CI, 1.10 to 2.07) for active smokers. Among quitters, the RR decreased as duration of cessation increased: With nonsmokers as the reference group, the RR for quitters was 1.62 (CI, 1.02 to 2.61) if the duration of cessation was 0 to less than 6 months, 1.60 (CI, 0.97 to 2.60) if the duration was 6 to less than 18 months, 1.48 (CI, 0.76 to 2.51) if the duration was 18 to less than 36 months, and 1.02 (CI, 0.54 to 1.86) if the duration was 36 months or more (P = 0.01 for trend). After incident myocardial infarction, smoking was associated with an elevated risk for recurrent coronary events. In persons who quit smoking after infarction, the risk declined to equal that of nonsmokers by 3 years after cessation.

Short-term hormone replacement therapy may increase the risk of recurrent coronary events, but long-term therapy reduces risk

Short-term hormone replacement therapy may increase the risk of recurrent coronary events, but long-term therapy reduces risk

Depression, Hostility, and Social Isolation in Patients with Coronary Artery Disease.

Psychosocial risk factors such as depression, hostility, and social isolation are substantially more prevalent in patients with coronary artery disease (CAD) than is widely recognized. It has been demonstrated that patients with CAD who have these risk factors, individually or together, may have a substantially increased risk for recurrent ischemic events, as well as cardiac death, when compared with unaffected CAD patients. Numerous adverse physiologic changes that appear to occur as a consequence of these psychosocial risk factors have been identified, including increased platelet aggregation, hyperadrenergic states, elevated cortisol levels, abnormal endothelial function, and an increased propensity towards malignant ventricular arrhythmias. Each of these may explain the increased risk of recurrent coronary events (including death) among afflicted patients. Under-recognition, and hence under-treatment, remains a principal obstacle for improvements in the care of patients with CAD who have psychosocial risk factors. The diagnosis of psychosocial risk factors depends on systematic patient evaluation by experienced clinicians trained in the recognition of these disorders. All clinicians must be aware of the potential importance of these factors, their sometimes subtle presenting characteristics, and the available treatment options. The universal use of comprehensive cardiovascular rehabilitation offers the ideal conduit for such evaluation and management. Nonpharmacologic therapies for psychosocial risk factors include psychotherapy, stress-reduction techniques, and exercise therapy. Studies suggest that the reduction of social isolation among depressed patients with CAD may result in a reduced mortality rate in comparison with those without improvements in isolation. Pharmacologic therapies are mainly for the management of depression, and largely center on the use of selective serotonin reuptake inhibitors (SSRIs). Several SSRIs (paroxetine and sertraline) recently have been shown to be safe and effective for the treatment of depression in patients with ischemic heart disease. Whether use of antidepressants attenuate the increased cardiac risk from depression in the setting CAD remains to be proven; however, their use improves the quality of life in properly selected patients.

Statin therapy, inflammation and recurrent coronary events in patients following coronary stent implantation

OBJECTIVESWe sought to investigate whether statin therapy affects the association between preprocedural C-reactive protein (CRP) levels and the risk for recurrent coronary events in patients undergoing coronary stent implantation.BACKGROUNDLow-grade inflammation as detected by elevated CRP levels predicts the risk of recurrent coronary events. The effect of inflammation on coronary risk may be attenuated by statin therapy.METHODSWe investigated a potential interrelation among statin therapy, serum evidence of inflammation, and the risk for recurrent coronary events in 388 consecutive patients undergoing coronary stent implantation. Patients were grouped according to the median CRP level (0.6 mg/dl) and to the presence of statin therapy.RESULTSA primary combined end point event occurred significantly more frequently in patients with elevated CRP levels without statin therapy (RR [relative risk] 2.37, 95% CI [confidence interval] [1.3 to 4.2]). Importantly, in the presence of statin therapy, the RR for recurrent events was significantly reduced in the patients with elevated CRP levels (RR 1.27 [0.7 to 2.1]) to about the same degree as in patients with CRP levels below 0.6 mg/dl and who did not receive statin therapy (RR 1.1 [0.8 to 1.3]).CONCLUSIONSStatin therapy significantly attenuates the increased risk for major adverse cardiac events in patients with elevated CRP levels undergoing coronary stent implantation, suggesting that statin therapy interferes with the detrimental effects of inflammation on accelerated atherosclerotic disease progression following coronary stenting.

Role of tumor necrosis factor-α and interleukin-6 in the effects of hormone replacement therapy and raloxifene on C-reactive protein in postmenopausal women

Observational studies 1 Cushman M Meilahn E.N Psaty B.M Kuller L.H Dobs A.S Tracy R.P Hormone replacement therapy, inflammation, and hemostasis in elderly women. Arterioscler Thromb Vasc Biol. 1999; 19: 893-899 Crossref PubMed Scopus (220) Google Scholar , 2 Ridker P.M Hennekens C.H Rifai N Buring J.E Manson J.E Hormone replacement therapy and increased plasma concentration of C-reactive protein. Circulation. 1999; 100: 713-716 Crossref PubMed Scopus (424) Google Scholar and randomized trials 3 van Baal W.M Kenemans P van der Mooren M.J Kessel H Emeis J.J Stehouwer C.D Increased C-reactive protein levels during short-term hormone replacement therapy in healthy postmenopausal women. Thromb Haemost. 1999; 81: 925-928 PubMed Google Scholar , 4 Cushman M Legault C Barrett-Connor E Stefanick M.L Kessler C Judd H.L Sakkinen P.A Tracy R.P Effect of postmenopausal hormones on inflammation-sensitive proteins The postmenopausal Estrogen/Progestin interventions (PEPI) study. Circulation. 1999; 100: 717-722 Crossref PubMed Scopus (621) Google Scholar have demonstrated that estrogen therapy with and without concomitant progestin increases the serum level of C-reactive protein (CRP) in postmenopausal women. CRP, a circulating marker of inflammation, is an independent risk factor for cardiovascular events in healthy postmenopausal women. 5 Ridker P.M Hennekens C.H Buring J.E Rifai N C-reactive protein and other markers of inflammation in the prediction of cardiovascular disease in women. N Engl J Med. 1999; 342: 836-843 Crossref Scopus (4967) Google Scholar The serum concentration of CRP correlates with that of tumor necrosis factor-α (TNF-α) 6 Ridker P.M Rifai N Pfeffer M Sacks F Lepage S Braunwald E Elevation of tumor necrosis factor-alpha and increased risk of recurrent coronary events after myocardial infarction. Circulation. 1999; 101: 2149-2153 Crossref Scopus (824) Google Scholar and interleukin-6 (IL-6), 7 Ridker P.M Rifai N Stampfer M.J Hennekens C.H Plasma concentration of interleukin-6 and the risk of future myocardial infarction among apparently healthy men. Circulation. 1999; 101: 1767-1772 Crossref Scopus (1986) Google Scholar the primary stimulant of hepatic CRP production. 8 Baumann H Gauldie J The acute phase response. Immunol Today. 1999; 15: 74-80 Abstract Full Text PDF Scopus (428) Google Scholar Raloxifene is a selective estrogen receptor modulator used clinically for the prevention and treatment of postmenopausal osteoporosis, 9 Kauffman R.F Bryant H.U Yang N Harper K Huster W.J Walls E Lufkin E.G Preventing postmenopausal osteoporosis An update on raloxifene. Drug News Perspect. 1999; 12: 223-233 Google Scholar and is also under investigation for its effect on the risk of major cardiovascular events in postmenopausal women. 10 Barrett-Connor E Wenger N.K Grady D Mosca L Collins P Kornitzer M Cox D.A Moscarelli E Anderson P.W Hormone and nonhormone therapy for the maintenance of postmenopausal health The need for randomized controlled trials of estrogen and raloxifene. J Women’s Health. 1999; 7: 839-847 Crossref Scopus (70) Google Scholar Unlike estrogen, raloxifene does not increase CRP levels in postmenopausal women, 11 Walsh B.W Paul S Wild R.A Dean R.A Tracy R.P Cox D.A Anderson P.W The effects of hormone replacement therapy and raloxifene on C-reactive protein and homocysteine in healthy postmenopausal women A randomized, controlled trial. J Endocrinol Metabol. 1999; 85: 214-218 Google Scholar , 12 Blum A Schenke W.H Hathaway L Mincemoyer R Csako G Waclawiw M.A Cannon R.O Effects of estrogen and the selective estrogen receptor modulator raloxifene on markers of inflammation in postmenopausal women. Am J Cardiol. 1999; 86: 892-895 Abstract Full Text Full Text PDF Scopus (37) Google Scholar although the mechanism for this difference remains unclear. We hypothesized that the differing effects of hormone replacement therapy (HRT) and raloxifene on serum CRP concentrations may be due to different effects on selected proinflammatory cytokines, such as IL-6 and TNF-α. This study compared the effects of HRT and raloxifene on the serum concentrations of TNF-α and IL-6, and assessed the relation between these effects and changes in serum CRP observed in the same population of postmenopausal women.

Body mass index and the risk of recurrent coronary events following acute myocardial infarction

Although excess adiposity appears to increase the risk of coronary heart disease in the general population, its importance in patients with established coronary disease is less defined. We evaluated a population-based inception cohort of survivors to hospital discharge following first acute myocardial infarction (AMI) (n = 2,541) to assess the association between body mass index (BMI) and the risk of recurrent coronary events and to explore the mechanisms for this relation. Using Cox proportional-hazards regression, we assessed the risk of recurrent coronary events associated with levels of adiposity as defined by BMI and then investigated potential mechanisms through which adiposity conferred risk by examining how adjustment for diabetes mellitus, systemic hypertension, and dyslipidemia affected the association. Forty-one percent of the cohort were overweight (BMI 25 to 29.9), and 27.8% were obese (BMI ≥30). After adjustment for other risk factors, the risk of recurrent coronary events (n = 418) increased as BMI increased, especially among those who were obese. Using a BMI of 16 to 24.9 as the reference group, for mildly overweight patients (BMI 25 to 27.4), the relative risk (RR) was 0.93 (95% confidence interval [CI] 0.70 to 1.24); it was 1.16 for more severe overweight patients (BMI 27.5 to 29.9; 95% CI 0.87 to 1.55). For patients with class I obesity (BMI 30 to 34.9), the RR was 1.49 (95% CI 1.12 to 1.98), and for class II to III obesity (BMI ≥35), the RR was 1.80 (95% CI 1.30 to 2.48). We estimated that clinical measurements of diabetes, hypertension, and dyslipidemia explained approximately 43% of this risk. Thus, excess adiposity as measured by BMI was associated with an increased risk of recurrent coronary events following AMI, particularly among those who were obese.

Risk of recurrent coronary events in relation to use and recent initiation of postmenopausal hormone therapy.

The finding from the Heart and Estrogen/Progestin Replacement Study (HERS) of increased coronary risk restricted to the first year after starting postmenopausal hormone therapy raises new questions about the role of hormone therapy in women with coronary heart disease. We assessed the risk of recurrent myocardial infarction or coronary heart disease death associated with the use and recent initiation of hormone therapy in women who survived a first myocardial infarction. The setting for this population-based inception cohort study was Group Health Cooperative, a health maintenance organization. We studied 981 postmenopausal women who survived to hospital discharge after their first myocardial infarction between July 1, 1986, and December 31, 1996. We obtained information on hormone use from the Group Health Cooperative computerized pharmacy database and identified recurrent coronary events by medical record review. During median follow-up of 3.5 years, there were 186 recurrent coronary events. There was no difference in the risk of recurrent coronary events between current users of hormone therapy and other women (adjusted relative hazard [RH], 0.96; 95% confidence interval [CI], 0.62-1.50). Relative to the risk in women not currently using hormones, there was a suggestion of increased risk during the first 60 days after starting hormone therapy (RH, 2.16; 95% CI, 0.94-4.95) and reduced risk with current hormone use for longer than 1 year (RH, 0.76; 95% CI, 0.42-1.36). These results are consistent with the findings from the HERS, suggesting a transitory increase in coronary risk after starting hormone therapy in women with established coronary heart disease and a decreased risk thereafter.

Elevation of tumor necrosis factor-alpha and increased risk of recurrent coronary events after myocardial infarction.

Levels of tumor necrosis factor-alpha (TNF-alpha) increase with acute ischemia. However, whether elevations of TNF-alpha in the stable phase after myocardial ischemia (MI) are associated with increased risk of recurrent coronary events is unknown. A nested case-control design was used to compare TNF-alpha levels obtained an average of 8.9 months after initial MI among 272 participants in the Cholesterol And Recurrent Events (CARE) trial who subsequently developed recurrent nonfatal MI or a fatal cardiovascular event (cases) and from an equal number of age- and sex-matched participants who remained free of these events during follow-up (controls). Overall, TNF-alpha levels were significantly higher among cases than controls (2.84 versus 2.57 pg/mL, P=0.02). The excess risk of recurrent coronary events after MI was predominantly seen among those with the highest levels of TNF-alpha, such that those with levels in excess of 4.17 pg/mL (the 95th percentile of the control distribution) had an approximately 3-fold increase in risk (RR=2.7, 95% CI 1.4 to 5.2, P=0.004). Risk estimates were independent of other risk factors and were similar in subgroup analyses limited to cardiovascular death (RR=2.1) or to recurrent nonfatal MI (RR=3.2). Plasma concentrations of TNF-alpha are persistently elevated among post-MI patients at increased risk for recurrent coronary events. These data support the hypothesis that a persistent inflammatory instability is present among stable patients at increased vascular risk. Novel therapies designed to attenuate inflammation may thus represent a new direction in the treatment of MI.

Thrombogenic factors and recurrent coronary events.

Thrombosis is a pivotal event in the pathogenesis of coronary disease. We hypothesized that the presence of blood factors that reflect enhanced thrombogenic activity would be associated with an increased risk of recurrent coronary events during long-term follow-up of patients who have recovered from myocardial infarction. We prospectively enrolled 1045 patients 2 months after an index myocardial infarction. Baseline thrombogenic blood tests included 6 hemostatic variables (D-dimer, fibrinogen, factor VII, factor VIIa, von Willebrand factor, and plasminogen activator inhibitor-1), 7 lipid factors [cholesterol, triglycerides, HDL cholesterol, LDL cholesterol, lipoprotein(a), apolipoprotein (apo)A-I, and apoB], and insulin. Patients were followed up for an average of 26 months, with the primary end point being coronary death or nonfatal myocardial infarction, whichever occurred first. The hemostatic, lipid, and insulin parameters were dichotomized into their top and the lower 3 risk quartiles and evaluated for entry into a Cox survivorship model. High levels of D-dimer (hazard ratio, 2.43; 95% CI, 1.49, 3.97) and apoB (hazard ratio, 1.82; 95% CI, 1.10, 3.00) and low levels of apoA-I (hazard ratio, 1.84; 95% CI, 1.10, 3.08) were independently associated with recurrent coronary events in the Cox model after adjustment for 6 relevant clinical covariates. Our findings indicate that a procoagulant state, as reflected in elevated levels of D-dimer, and disordered lipid transport, as indicated by low apoA-1 and high apoB levels, contribute independently to recurrent coronary events in postinfarction patients.

Antibiotics for myocardial infarction? A possible role of infection in atherogenesis and acute coronary syndromes.

The role of inflammatory mechanisms in the initiation, progression and clinical expression of atherosclerosis is increasingly appreciated. With this awareness, the possibility that acute or chronic infection may initiate or modulate these processes in an active area of investigation. Infectious organisms may influence the atherosclerotic process through direct local effects on the coronary endothelium, on vascular smooth muscle cells and on macrophages in the atherosclerotic lesion. Infection may also exert systemic effects by inducing the elaboration of cytokines, the creation of a hypercoagulable state and by activating monocytes, causing possible transmission of infectious material to atherosclerotic lesions. Macrophages may then elaborate multiple mediators which destabilise plaque, promoting rupture and progression. Seroepidemiological data have identified associations between clinically active atherosclerosis and evidence of infection with Helicobacter pylori, Chlamydia pneumoniae and some herpesviridae. In addition, pathological examinations have demonstrated the presence of infectious organisms in coronary artery plaques. Cytomegalovirus, for example, has been identified pathologically to be associated with transplant vasculopathy and with an increased risk of restenosis following coronary intervention. Finally, recent pilot trials have demonstrated that macrolide antibacterial treatment directed against C. pneumoniae reduces the risk of recurrent coronary events. Infectious organisms may therefore influence atherogenesis through multiple pathways, and pathological and seroepidemiological investigations provide evidence of this association. Future large-scale clinical trials are needed to further evaluate the evidence of causality and the efficacy of antibacterial therapy for coronary artery disease.

Inflammation, Pravastatin, and the Risk of Coronary Events After Myocardial Infarction in Patients With Average Cholesterol Levels

We studied whether inflammation after myocardial infarction (MI) is a risk factor for recurrent coronary events and whether randomized treatment with pravastatin reduces that risk. A nested case-control design was used to compare C-reactive protein (CRP) and serum amyloid A (SAA) levels in prerandomization blood samples from 391 participants in the Cholesterol and Recurrent Events (CARE) trial who subsequently developed recurrent nonfatal MI or a fatal coronary event (cases) and from an equal number of age- and sex-matched participants who remained free of these events during follow-up (control subjects). Overall, CRP and SAA were higher among cases than control subjects (for CRP P=0.05; for SAA P=0.006) such that those with levels in the highest quintile had a relative risk (RR) of recurrent events 75% higher than those with levels in the lowest quintile (for CRP RR= 1.77, P=0.02; for SAA RR= 1.74, P=0.02). The study group with the highest risk was that with consistent evidence of inflammation (elevation of both CRP and SAA) who were randomly assigned to placebo (RR=2.81, P=0.007); this risk estimate was greater than the product of the individual risks associated with inflammation or placebo assignment alone. In stratified analyses, the association between inflammation and risk was significant among those randomized to placebo (RR=2.11, P=0.048) but was attenuated and nonsignificant among those randomized to pravastatin (RR=1.29, P=0.5). Evidence of inflammation after MI is associated with increased risk of recurrent coronary events. Therapy with pravastatin may decrease this risk, an observation consistent with a nonlipid effect of this agent.

Echocardiographic left ventricular systolic function and volumes in young adults: Distribution and factors influencing variability

Low left ventricular ejection fraction (LVEF), a measure of global systolic left ventricular dysfunction, is associated with an increased risk of recurrent coronary events or death in persons with cardiac disease. There are few data on the distribution of resting LVEF and component volumes in healthy young adults or on any associaton of LVEF with coronary risk factors. LVEF and left ventricular end-diastolic and end-systolic volumes (LVEDV and LVESV, respectively) were measured by two-dimensional echocardiography in 1782 men and women 23 to 35 years old without self-reported heart disease (other than mitral valve prolapse, n = 53) who were participants in the multicenter Coronary ARtery Risk Development in Young Adults study. Factors analyzed as potential contributors to LVEF, LVEDV, and LVESV included age, gender, race, blood pressure, alcohol use, current smoking, family history of myocardial infarction, total and high-density lipoprotein cholesterol concentrations, obesity, reported physical activity, and fitness as assessed by treadmill exercise testing. LVEF was lower in men (mean 62.6%, SD 5.7%) than in women (mean 63.9%, SD 5.7%), ( p < 0.01) but did not differ significantly between black and white subjects. Ninety percent of subjects had an LVEF between 53% and 71%. LVEDV and LVESV were >25% greater in men than in women. From multivariate analysis, male gender, history of hypertension, and current smoking were each positively and independently associated with an approximately 1% lower LVEF. Body surface area, a family history of premature myocardial infarction, and treadmill workload 150 time were positively related, whereas total skinfold thickness was negatively related to LVEDV and LVESV. In addition, systolic blood pressure was positively related and diastolic blood pressure and total cholesterol concentration negatively refated to LVEDV, whereas treadmill performance measured in metabolic equivalents (METS) and current smoking were positively related and age negatively related to LVESV. These results suggest that LVEF in healthy young adults is maintained over a limited range and that is variability not substantially associated with coronary risk factors. Determination of whether differences in LVEF, LVESV, and LVEDV in young adults influence future cardiovascular risk and whether obesity and other factors express any effect on risk through differences in LVESV and LVEDV will require longitudinal follow-up studies.

Cost-effectiveness of HMG-CoA Reductase Inhibition for Primary and Secondary Prevention of Coronary Heart Disease

To determine the cost-effectiveness of HMG-CoA (3-hydroxy-3-methylglutaryl coenzyme A) reductase inhibitors (such as lovastatin) for the primary and secondary prevention of coronary heart disease, we used the Coronary Heart Disease Policy Model, a computer-stimulated model that estimates the risk factor-specific annual incidence of coronary heart disease and the risk of recurrent coronary events in persons with prevalent coronary heart disease. When used for secondary prevention, 20 mg/d of lovastatin was estimated to save lives and save costs in younger men with cholesterol levels above 250 mg/dL (6.47 mmol/L) and to have a favorable cost-effectiveness ratio regardless of the cholesterol level except in young women with cholesterol levels below 250 mg/dL (6.47 mmol/L). Doses of 40 mg/d of lovastatin had favorable incremental cost-effectiveness ratios in men with cholesterol levels above 250 mg/dL (6.47 mmol/L). By comparison, primary prevention had favorable cost-effectiveness ratios only in selected subgroups based on cholesterol levels and other established risk factors. We conclude that current national recommendations regarding medication for secondary prevention are not as aggressive as our projections would suggest, while recommendations regarding the use of medications for primary prevention should consider the cost of medication as well as the risk factor profile of the individual patient.

Comparison of early exercise treadmill test and oral dipyridamole thallium-201 tomography for the identification of jeopardized myocardium in patients receiving thrombolytic therapy for acute Q-wave myocardial infarction

Thrombolytic therapy has become the treatment of choice for patients with acute myocardial infarction. Researchers are not yet able to identify patients with salvage of myocardium who are at risk for recurrent coronary events. Thus, a prospective trial was performed in 46 patients with myocardial infarction (28 anterior and 18 inferior) who received thrombolytic therapy to determine if early thallium tomography (4.7 days) using oral dipyridamole would identify more patients with residual ischemia than early symptom-limited exercise treadmill tests (5.5 days). There were no complications during the exercise treadmill tests or oral dipyridamole thallium tomography. Mean duration of exercise was 11 ± 3 minutes and the peak heart rate was 126 beats/min. Thirteen patients had positive test results. After oral dipyridamole all patients had abnormal thallium uptake on the early images. Positive scans with partial “filling in” of the initial perfusion defects were evident in 34 patients. Angina developed in 13 patients and was easily reversed with intravenous aminophylline. Both symptom-limited exercise treadmill tests and thallium tomography using oral dipyridamole were safely performed early after myocardial infarction in patients receiving thrombolytic therapy. Thallium tomography identified more patients with residual ischemia than exercise treadmill tests (74 vs 28%). Further studies are required to determine whether the results of thallium tomography after oral dipyridamole can be used to optimize patient management and eliminate the need for coronary angiography in some patients.

Risk factors for long-term coronary prognosis after initial myocardial infarction: the Framingham Study.

The role of standard coronary heart disease risk factors in predicting the long-term risk of recurrent coronary events in survivors of myocardial infarction is examined. Of 697 subjects (464 males and 233 females) who experienced an initial myocardial infarction during 30 years of follow-up in the Framingham Study, 459 returned for a baseline examination and were followed for up to 32 years (mean = 9.7 years) for incident reinfarction or coronary death. The Cox proportional hazards model was used to evaluate the relation of postinfarction risk factors with reinfarction and coronary death. Age-adjusted analyses showed the risk of reinfarction to be positively associated with blood pressure and serum cholesterol. Risk of coronary death was strongly associated with blood sugar level, systolic blood pressure, serum cholesterol, heart rate, diabetes, and interim reinfarction. In multivariable analyses, systolic pressure, serum cholesterol, and diabetes were predictive of reinfarction; relative weight was inversely associated with reinfarction. Systolic pressure, serum cholesterol, and the prevalence of diabetes persisted as independent predictors of coronary death. When adjustments were made for the effects of these variables, women were at only half the risk of coronary death compared with men. Higher baseline risk factors in women compared with men may obscure an important survival advantage in women. In persons recovered from an initial myocardial infarction, standard risk factors, particularly systolic pressure, serum cholesterol, and diabetes, remain important determinants of coronary prognosis over many years and warrant attention in preventing subsequent events.

Repeat coronary angioplasty for restenosis: Results and predictors of follow-up clinical events

To determine the predictors of long-term outcome after repeat percutaneous transluminal coronary angioplasty (PTCA), we analyzed the immediate and follow-up results of 144 patients who underwent a second PTCA procedure for restenosis of a previously successfully dilated lesion. Clinical success was obtained in 94% of patients. Emergency coronary bypass graft surgery was required in two patients (1%). Of the 136 successfully treated patients, 126 were followed for a duration of 6 to 36 months (mean 16, median 12 months). The follow-up coronary events (mutually exclusive) included cardiac death (2%), nonfatal myocardial infarction (2%), coronary bypass surgery (15%), and third PTCA (9%). According to results of Cox regression analysis, the independent variables associated with an increased risk of recurrent coronary events after repeat PTCA were: dilatation of a proximal left anterior descending artery stenosis at both initial and second PTCA ( p = 0.001), time interval between the initial and the second PTCA ≤3 months ( p = 0.001), multiple versus single-lesion redilatation at the time of repeat PTCA ( p = 0.002), and the presence of diabetes mellitus ( p = 0.005). Thus repeat PTCA for restenosis is a safe and efficacious procedure, and it provides excellent long-term outcome in the majority of patients. Dilatation of a proximal left anterior descending artery lesion, a short time interval between the first and second PTCA procedures, diabetes mellitus, and redilatation of multiple lesions are predictors of recurrent clinical events after a second PTCA. Repeat PTCA should be considered carefully for patients falling within a high-risk profile for recurrent events after the procedure.

High Dose Statins: Is it Beneficial over Conventional Dose of Statin in Acute Coronary Syndrome?

Increasing burden of cardiovascular disease risk factors has led to increase in the incidence in the coronary artery disease (CAD). Advancements in medical and surgical care of patients with heart disease have led to a large number of people surviving acute coronary events. Patients with acute coronary syndrome (ACS) are at high risk for recurrent coronary events, sudden death, and all cause mortality. Conventional revascularization therapies reduce the risk of further ischaemia but do not affect the underlying atherosclerotic disease. Statins have a proven record in the secondary prevention of coronary heart disease. Furthermore, statins have been shown to exert various pleotropic effects, which may stabilize vulnerable atherosclerotic plaques. Therefore, initiating, statin therapy in patients with established CAD is both beneficial and more cost effective. Trials conducted in recent times have addressed the issue of whether higher dose statin therapy provides further reductions in the risks of cardiovascular events following an acute coronary syndrome diagnosis, over and above that provided by a conventional dose statin regimen. However, recent trials of high dose statin therapy in patients with acute coronary syndromes have yielded conflicting results. The aim of this article is to provide a critical and up-to-date summary of the findings of clinical trials of intensive statin therapy, including a brief overview of safety and efficacy of such treatments. Keywords: Statin; Acute coronary syndrome. DOI: 10.3329/cardio.v2i2.6648Cardiovasc. j. 2010; 2(2) : 245-251