N-terminal probrain natriuretic peptide and C-reactive protein in stable coronary heart disease

Purpose

C-reactive protein (CRP) and N-terminal pro-brain natriuretic peptide (NT-proBNP) provide prognostic information in patients with stable coronary heart disease. The aim of the study was to investigate whether combined use of NT-proBNP and CRP improves risk stratification in these patients.

Methods

This cohort study included 989 patients with stable coronary heart disease who underwent coronary stenting. CRP and NT-proBNP were measured before angiography. The primary end point of the study was all-cause mortality. Using median values of NT-proBNP (279.9 ng/L) and CRP (1.2 mg/L), patients were divided into 4 groups: low NT-proBNP-low CRP group (305 patients with NT-proBNP<median and CRP<median); low NT-proBNP-high CRP group (190 patients with NT-proBNP<median and CRP≥median; high NT-proBNP-low CRP group (237 patients with NT-proBNP≥median and CRP<median); and high NT-proBNP-high CRP group (257 patients with NT-proBNP≥median and CRP≥median).

Results

During a median follow-up of 3.6 years (interquartile range 3.3 to 4.5 years), there were 85 deaths: 6 deaths in the low NT-proBNP-low CRP group, 11 deaths in the low NT-proBNP-high CRP group, 20 deaths in the high NT-proBNP-low CRP group, and 48 deaths in the high NT-proBNP-high CRP group with Kaplan-Meier mortality estimates of 2.7%, 8.9%, 12.1% and 35.6%, respectively (P <.001). Cox proportional hazards model showed that combination NT-proBNP-CRP was the strongest independent correlate of mortality (hazard ratio [HR] 4.3, 95% confidence interval [CI], 2.0-9.3; P <.001 for high NT-proBNP-high CRP vs low NT-proBNP-low CRP).

Conclusion

Combined use of NT-proBNP and CRP improves long-term risk prediction of mortality in patients with stable coronary heart disease.     

Risk Factors for Heart Failure: A Population-Based Case-Control Study

Background

The relative contribution of risk factors to the development of heart failure remains controversial. Further, whether these contributions have changed over time or differ by sex is unclear. Few population-based studies have been performed. We aimed to estimate the population attributable risk (PAR) associated with key risk factors for heart failure in the community.

Methods

Between 1979 and 2002, 962 incident heart failure cases in Olmsted County were age and sex-matched to population-based controls using Rochester Epidemiology Project resources. We determined the frequency of risk factors (coronary heart disease, hypertension, diabetes mellitus, obesity, and smoking), odds ratios, and PAR of each risk factor for heart failure.

Results

The mean number of risk factors for heart failure per case was 1.9 ± 1.1 and increased over time (P <.001). Hypertension was the most common (66%), followed by smoking (51%). The prevalence of hypertension, obesity, and smoking increased over time. The risk of heart failure was particularly high for coronary disease and diabetes with odds ratios (95% confidence intervals) of 3.05 (2.36-3.95) and 2.65 (1.98-3.54), respectively. However, the PAR was highest for coronary disease and hypertension; each accounted for 20% of heart failure cases in the population, although coronary disease accounted for the greatest proportion of cases in men (PAR 23%) and hypertension was of greatest importance in women (PAR 28%).

Conclusion

Preventing coronary disease and hypertension will have the greatest population impact in preventing heart failure. Sex-targeted prevention strategies might confer additional benefit. However, these relationships can change, underscoring the importance of continued surveillance of heart failure.     

Activation of the inflammation, coagulation, and fibrinolysis systems, without influence of abciximab infusion in patients with non-ST-elevation acute coronary syndromes treated with dalteparin: a GUSTO IV substudy

Background

In acute coronary syndromes, the inflammation and the coagulation systems are activated, implying an impaired outcome. In addition to platelet inhibition, recent evidence suggests that the glycoprotein IIb/IIIa receptor inhibitor abciximab attenuates inflammation and coagulation activity.

Methods

The Swedish Global Utilization of Strategies To open Occluded arteries-IV (GUSTO-IV) substudy included 404 patients with non-ST-elevation acute coronary syndromes. In addition to aspirin and dalteparin, all patients were randomized to receive abciximab infusion for 24 hours or 48 hours or corresponding placebo without early coronary revascularization. Plasma samples were obtained at baseline and 24, 48, and 72 hours.

Results

The median levels of the coagulation markers thrombin/antithrombin complex and soluble fibrin increased significantly from 3.1 to 3.7 ug/L (baseline to peak; P <.001) and from 20 to 23 nmol/L (P <.001), respectively. The fibrinolysis marker, tissue plasminogen-activator, also increased its median levels, from 11.7 to 17.5 ug/L (P <.001), whereas the median level of plasminogen-activator-inhibitor was unchanged. The inflammatory markers interleukin-6, C-reactive protein, and fibrinogen also increased their median levels (5.4-7.8 ng/L, P <.001; 4.4-8.7 mg/L, P <.001; 3.3-3.9 g/L, P <.001). However, there were no differences in median levels or in changes of median levels of any marker at any point between the placebo group and any of the abciximab groups.

Conclusions

In non-ST-elevation acute coronary syndrome, there was a simultaneous activation of the inflammation, coagulation, and fibrinolysis systems, despite aspirin and dalteparin treatment. Prolonged treatment with abciximab had no influence of the activation of these systems.     

Predictors and Implications of Q-Waves in ST-Elevation Acute Coronary Syndromes

Background

Q-waves in ST-elevation acute coronary syndromes carry adverse implications. We sought to determine the frequency, predictors, and implications of Q-waves in the current era that includes primary percutaneous coronary interventions.

Methods

There were 14,916 patients evaluated in a multicenter observational study. They presented with ST-elevation acute coronary syndromes between 1999 and 2006. Clinical variables were compared between patients with versus without presenting Q-waves, with an additional comparison in the latter group between those with versus without subsequent development of Q-waves.

Results

ST-elevation myocardial infarction occurred in 88.6% of patients. Q-waves were present on the initial electrocardiogram in 3929 patients and developed later in an additional 3085 patients. The incidence of Q-waves at presentation or during hospitalization decreased from 61% to 39% between 1999 and 2006 (linear trend P < .001). Both presenting and subsequent Q-waves were associated with greater likelihood of coronary occlusions and higher cardiac marker elevations (P <.001). Multivariate analysis showed that presenting Q-waves were associated with male sex (odds ratio [OR] 1.28), increased age (OR 1.06 per 5 years), diabetes (OR 1.26), smoking (OR 1.11), chronic aspirin (OR 0.79), acute aspirin (OR 0.87), other chronic cardiac medications (OR 0.80), prior heart failure (OR 0.67), and prior coronary artery disease (OR 0.61). Presenting Q-waves were independently associated with increased in-hospital mortality (OR 1.46), but Q-waves at presentation or during hospitalization did not impact 6-month mortality.

Conclusions

Q-waves in ST-elevation acute coronary syndromes are decreasing in incidence. Q-waves are a major determinant of in-hospital mortality, and targeted interventions should be directed to these high-risk patients.     

Prognostic implications of ejection fraction from linear echocardiographic dimensions: the Strong Heart Study

Background

Although echocardiography is commonly used to assess left ventricular (LV) systolic function, few data are available concerning the prognostic significance of LV ejection fraction (EF) calculated from linear echocardiographic measurements or 2-dimensional (2-D) wall motion scores in population-based samples.

Methods

Echocardiography was used in the second Strong Heart Study (SHS) examination to calculate LV EF in 2948 American Indians without prevalent coronary heart disease; 2923 had 2-D wall motion scores.

Results

Mildly and severely reduced LV EF occurred in 10% and 2% of participants, was associated with older age, male sex, higher systolic pressure, heart rate and markers of renal disease and inflammation. During 37 ± 9 months follow-up, cardiovascular death occurred in 2%, 5% and 12% of participants with normal, mildly reduced and severely reduced EF; all cause mortality rates were 6%, 10% and 32% (both P < .001). In Cox proportional hazards analyses, adjusting for covariates, cardiovascular death was higher with mildly reduced EF (risk ratio [RR] 2.9, 95% CI 1.6-5.4, P = .0007) and especially with severely reduced EF (RR 6.9, 95% CI 3.0-15.9, P < .0001); all-cause mortality was increased with severe LV dysfunction (RR 4.8, 95% CI 2.8-8.1, P < .001) and marginally with mildly reduced EF (odds ratio 1.4, 95% CI 0.95-2.15, P = .08). Segmental LV dysfunction and mildly and severely reduced EF from 2-D wall motion scores were associated with 3.3-fold (95% CI 1.1-9.4, P = .02), 3.5-fold (95% CI 2.1-5.8) and 3.8-fold (95% CI 1.9-7.6) (all P < .001) increased rates of cardiovascular death.

Conclusions

LV EF from linear echocardiographic measurements as well as segmental LV dysfunction and EF from 2-D wall motion scores strongly and independently predict cardiovascular mortality. Reduced EF by simple echocardiographic method has estimated population-attributable risks of about 35% for cardiovascular death and 12% for all-cause mortality in a population-based sample of middle-aged to elderly adults.     

Aspirin resistance and adverse clinical events in patients with coronary artery disease

Purpose

We sought to determine the clinical significance of aspirin resistance measured by a point-of-care assay in stable patients with coronary artery disease (CAD).

Methods

We used the VerifyNow Aspirin (Accumetrics Inc, San Diego, Calif) to determine aspirin responsiveness of 468 stable CAD patients on aspirin 80 to 325 mg daily for ≥4 weeks. Aspirin resistance was defined as an Aspirin Reaction Unit ≥550. The primary outcome was the composite of cardiovascular death, myocardial infarction (MI), unstable angina requiring hospitalization, stroke, and transient ischemic attack.

Results

Aspirin resistance was noted in 128 (27.4%) patients. After a mean follow-up of 379 ± 200 days, patients with aspirin resistance were at increased risk of the composite outcome compared to patients who were aspirin-sensitive (15.6% vs 5.3%, hazard ratio [HR] 3.12, 95% confidence intervals [CI], 1.65-5.91, P < .001). Cox proportional hazard regression modeling identified aspirin resistance, diabetes, prior MI, and a low hemoglobin to be independently associated with major adverse long-term outcomes (HR for aspirin resistance 2.46, 95% CI, 1.27-4.76, P = .007).

Conclusions

Aspirin resistance, defined by an aggregation-based rapid platelet function assay, is associated with an increased risk of adverse clinical outcomes in stable patients with CAD.     

Coronary Heart Disease and Stroke Risk in Patients with Psoriasis: Retrospective Analysis

Background

Past studies suggest an association between psoriasis and the risk of developing coronary heart disease. The objectives of this study were to estimate the 10-year risks of coronary heart disease and stroke in patients with moderate to severe psoriasis, to compare risks between patients and the general population, and to determine whether risk profiles are affected by disease severity.

Methods

Data were pooled from patients with moderate to severe psoriasis (Psoriasis Area and Severity Index [PASI] score ≥ 10) who were enrolled in Phase II (M02-528) or Phase III trials (Comparative Study of HUMIRA vs Methotrexate vs Placebo In PsOriasis PatieNts[CHAMPION], Randomized Controlled EValuation of Adalimumab Every Other Week Dosing in Moderate to Severe Psoriasis TriAL[REVEAL]) evaluating adalimumab. Risks of coronary heart disease and stroke were estimated using the Framingham risk score algorithm and a stroke risk function based on the Framingham Heart Study cohorts. To compare risks between patients with psoriasis and the general population, average population risks were imputed on the basis of age and gender. Wilcoxon rank-sum tests evaluated risk differences between patients with psoriasis and the general population and between patients with moderate psoriasis and patients with severe psoriasis.

Results

A total of 1591 patients were identified, including 1082 patients with PASI scores ≥ 10 and ≤ 20 and 509 patients with PASI scores > 20. Patients with PASI scores from 10 to 20 and PASI scores > 20 had similar 10-year risks of coronary heart disease (12.3% and 12.2%; P = .49) and stroke (8.3% and 8.7%; P = .28). Compared with the general population, 10-year risks of patients with psoriasis were 28% greater for coronary heart disease (P < .001) and 11.8% greater for stroke (P = .02).

Conclusion

Patients with moderate to severe psoriasis had increased risks of coronary heart disease and stroke compared with the general population.     

Association of the PURSUIT risk score with predischarge ejection fraction, angiographic severity of coronary artery disease, and mortality in a nonselected, community-based population with non-ST-elevation acute myocardial infarction

Background

The Platelet Glycoprotein IIb/IIIa in Unstable Angina: Receptor Suppression Using Integrilin Therapy (PURSUIT) risk score was derived from the PURSUIT trial population for 30-day mortality prediction.

Methods

The PURSUIT risk score was calculated for 337 consecutive Olmsted County residents with non-ST-elevation acute myocardial infarction admitted to the coronary care unit of our institution from 1988 through 1998. Predischarge ejection fraction (EF) measurement was available for 246 patients (73%). After excluding patients with prior coronary artery bypass graft surgery (n = 42), 219 patients (65%) had coronary angiography within 30 days of admission. Mortality at 30 days was 8.9%. Among 30-day survivors, mortality at 1 year was 7.9%.

Results

Mean age was 70 ± 13 years, and 37% of patients were women. Mean predischarge EF was 52% ± 16%. Patients with higher PURSUIT risk score had lower EF (P < .001). Three-vessel (≥70% stenosis in all 3 coronary arteries) or left main (≥50% stenosis) coronary artery disease was present in 60 of 219 patients (27%) who had coronary angiography. Higher PURSUIT risk score was associated with greater likelihood of 3-vessel or left main disease (P < .001). The PURSUIT risk score had very good predictive accuracy for both early (30-day, C-statistic = 0.78) and late (30-day to 1-year, C-statistic = 0.77) mortality.

Conclusions

The PURSUIT risk score correlates with EF, angiographic severity of coronary artery disease, and short- and long-term mortality of nonselected patients with non-ST-elevation acute myocardial infarction.     

Low-dose aspirin in patients with stable cardiovascular disease: a meta-analysis

Objective

Many recommendations for aspirin in stable cardiovascular disease are based on analyses of all antiplatelet therapies at all dosages and in both stable and unstable patients. Our objective was to evaluate the benefit and risk of low-dose aspirin (50-325 mg/d) in patients with stable cardiovascular disease.

Methods

Secondary prevention trials of low-dose aspirin in patients with stable cardiovascular disease were identified by searches of the MEDLINE database from 1966 to 2006. Six randomized trials were identified that enrolled patients with a prior myocardial infarction (MI) (n = 1), stable angina (n = 1), or stroke/transient ischemic attack (n = 4). A random effects model was used to combine results from individual trials.

Results

Six studies randomized 9853 patients. Aspirin therapy was associated with a significant 21% reduction in the risk of cardiovascular events (nonfatal MI, nonfatal stroke, and cardiovascular death) (95% confidence interval [CI], 0.72-0.88), 26% reduction in the risk of nonfatal MI (95% CI, 0.60-0.91), 25% reduction in the risk of stroke (95% CI, 0.65-0.87), and 13% reduction in the risk of all-cause mortality (95% CI, 0.76-0.98). Patients treated with aspirin were significantly more likely to experience severe bleeding (odds ratio 2.2, 95% CI, 1.4-3.4). Treatment of 1000 patients for an average of 33 months would prevent 33 cardiovascular events, 12 nonfatal MIs, 25 nonfatal strokes, and 14 deaths, and cause 9 major bleeding events. Among those with ischemic heart disease, aspirin was most effective at reducing the risk of nonfatal MI and all-cause mortality; however, among those with cerebrovascular disease, aspirin was most effective at reducing the risk of stroke.

Conclusion

In patients with stable cardiovascular disease, low-dose aspirin therapy reduces the incidence of adverse cardiovascular events and all-cause mortality, and increases the risk of severe bleeding.     

Comparative study of ambient air particles in patients hospitalized for heart failure and acute coronary syndrome

Introduction and objectives

Currently air pollution is considered as an emerging risk factor for cardiovascular disease. Our objective was to study the concentrations of particulate matter in ambient air and analyze their relationship with cardiovascular risk factors in patients admitted to a cardiology department of a tertiary hospital with the diagnosis of heart failure or acute coronary syndrome (ACS).

Methods

We analyzed 3950 consecutive patients admitted with the diagnosis of heart failure or ACS. We determined the average concentrations of different sizes of particulate matter (<10, <2.5, and <1 μm and ultrafine particles) from 1 day or up to 7 days prior to admission (1 to 7 days lag time).

Results

There were no statistically significant differences in mean concentrations of particulate matter <10, <2.5 and <1 μm in size in both populations. When comparing the concentrations of ultrafine particles of patients admitted due to heart failure and acute coronary syndrome, it was observed that the former had a tendency to have higher values (19 845.35 ± 8 806.49 vs 16 854.97 ± 8005.54 cm⁻³, P <.001). The multivariate analysis showed that ultrafine particles are a risk factor for admission for heart failure, after controlling for other cardiovascular risk factors (odds ratio = 1.4; confidence interval 95%, from 1.15 to 1.66 P = .02).

Conclusions

In our study population, compared with patients with ACS, exposure to ultrafine particles is a precipitating factor for admission for heart failure.Full English text available from: www.revespcardiol.org     

Troponin elevation in supraventricular tachycardia: primary dependence on heart rate

Background

It is known that some patients with supraventricular tachycardia (SVT) could have increased troponin levels without coronary artery disease.

Objectives

To compare the cardiovascular risk of patients admitted with SVT with troponin T elevation (T+ patients) versus those without (T- patients), to determine if the rise in troponin levels could be predicted, and to identify the right approach in T+ patients.

Methods

Retrospective database search of patients with SVT from 2002 to 2007 either with or without troponin T elevation at admission.

Results

Of the 73 study patients, there were 24 (32.9%) T+ patients and 49 (67.1%) T- patients. All except 5 T+ patients underwent either a stress test/MIBI or a coronary angiogram. Two noninvasive tests were positive and only 1 patient needed an angiogram and percutaneous coronary intervention; none of the other angiograms triggered any further treatment. Of the 49 T- patients, 11 had a noninvasive stress test; none of these tests was positive or triggered any further treatment. Compared with that of T- patients, the maximum heart rate was significantly higher in T+ patients (190.8 versus 170.3 beats per minute, P = .008). A correlation was found between the maximal heart rate during SVT and the level of troponin elevation (r = 0.637, P = .001).

Conclusions

SVT could be associated with a troponin elevation without any severe coronary artery disease. In most patients, either conservative management or noninvasive stratification seems to be sufficient; an invasive strategy could then be reserved only for high-risk patients who tested positive. The only clinical variable correlated with the troponin rise was a higher maximal heart rate during the SVT episode.     

Depression and Clinical Outcomes in Heart Failure: An OPTIMIZE-HF Analysis

Background

Depression is a risk factor of excessive morbidity and mortality in heart failure. We examined in-hospital treatment and postdischarge outcomes in hospitalized heart failure patients with a documented history of depression from the Organized Program to Initiate Lifesaving Treatment in Hospitalized Patients with Heart Failure.

Methods

We identified patient factors associated with depression history and evaluated the association of depression with hospital treatments and mortality, and early postdischarge mortality, emergency care, and rehospitalization.

Results

In 48,612 patients from 259 hospitals, depression history was present in 10.6% and occurred more often in females, whites, and those with common heart failure comorbidities, including chronic pulmonary obstructive disease (36% vs 27%), anemia (27% vs 16.5%), insulin-dependent diabetes mellitus (20% vs 16%), and hyperlipidemia (38% vs 31%), all P <.001. Patients with depression history were less likely to receive coronary interventions and cardiac devices, all P <.01; or be referred to outpatient disease management programs, P <.001. Length of hospital stay was longer with depression history (7.0 vs 6.4 days, P <.001). In 5791 patients followed-up at 60-90 days postdischarge, those with depression history had higher mortality (8.8% vs 6.4%; P = .025). After multivariable modeling, depression history remained a predictor of length of hospital stay, P <.001 and postdischarge mortality, P = .02.

Conclusions

Depression history at heart failure hospitalization may be a predictor of prolonged length of hospital stay, less use of cardiac procedures and postdischarge disease management, and increased 60-90 day mortality. Patients with depression might represent a vulnerable group in which improved use of evidence-based treatment should be considered.     

Effects of low-dose angiotensin II receptor blocker candesartan on cardiovascular events in patients with coronary artery disease

Objectives

The purpose of this study was to investigate the effects of angiotensin II receptor blockers on the prevention of cardiovascular events in patients with coronary artery disease (CAD).

Background

Angiotensin II may contribute to the pathogenesis of CAD. Long-term clinical trials have shown that blockade of the renin-angiotensin system can reduce cardiovascular events in patients with acute myocardial infarction complicated by heart failure.

Methods

Patients with a history of coronary intervention and no significant coronary stenosis on follow-up angiography 6 months after intervention were randomly assigned into a candesartan group (n = 203; baseline treatment plus candesartan 4 mg/d) or a control group (n = 203; baseline treatment alone). The primary end point was a composite of revascularization, nonfatal myocardial infarction, or cardiovascular death. The secondary end point was hospitalization for cardiovascular causes.

Results

There were no changes in blood pressure and in other coronary risk factors in either group during a mean follow-up of 24 months. Primary end point risk was significantly lower in the candesartan group (n = 12) than in control group patients (n = 25) (P = .03). Candesartan treatment reduced primary end point risk (5.9% vs 12.3% for control subjects; relative risk, 0.47; 95% CI, 0.24 to 0.93). The incidence of all events including secondary end points and noncardiovascular death was significantly lower in the candesartan group than in control group patients (23 vs 40 cases) (P = .02).

Conclusions

Relatively low-dose candesartan, which did not alter blood pressure levels, reduces cardiovascular risk in high-risk patients with CAD.     

Prognostic value of predischarge electrocardiographic measurement of infarct size after thrombolysis: insights from GUSTO I Economics and Quality of Life substudy

Background

Current methods for risk stratification after acute myocardial infarction (MI) include several noninvasive studies. In this cost-containment era, the development of low-cost means should be encouraged. We assessed the ability of an electrocardiogram (ECG) MI-sizing score to predict outcomes in patients enrolled in the Economics and Quality of Life (EQOL) sub study of the Global Utilization of Streptokinase and Tissue plasminogen activator for Occluded coronary arteries -I (GUSTO-I) trial.

Methods

We classified patients by electrocardiographic Selvester QRS score at hospital discharge: those with a score 0-9 versus ≥10. Endpoints were 30-day and 1-year mortality, resource use, and quality-of-life measures.

Results

Patients with a QRS score <10 were well-matched with those with QRS score ≥10 with the exception of a trend to more anterior MI in the higher scored group. Patients with QRS score ≥10 had increased risk of death at 30-days (8.9% vs. 2.9% P < .001), and this difference persisted at 1 year (12.6% vs. 5.4%, P = .001). Recurrent chest pain, use of angiography, and angioplasty were similar during follow-up. However, there was a trend toward less coronary bypass surgery in patients with a QRS score ≥10. Readmission rates were higher at 30 days but similar at 1 year.

Conclusions

Stratification of patients after acute MI by a simple measure of MI size identifies populations with different long-term prognoses; patients with a QRS score ≥10 (approximately 30% of the left ventricle infarcted) at discharge have poorer outcomes in both the short- and long-term. The standard 12-lead ECG provides a simple, economical means of risk stratification at discharge.     

Too little aspirin for secondary prevention after acute myocardial infarction in patients at high risk for cardiovascular events: Results from the MITRA study

Background

A meta-analysis of randomized trials has shown a significant reduction of mortality rate in patients receiving aspirin for secondary prevention after acute myocardial infarction (AMI). However, a significant number of patients do not receive aspirin after AMI. Little is known about why aspirin is withheld or the long-term outcome of these patients today.

Methods

The Maximal Individual Therapy in Acute Myocardial Infarction (MITRA) registry is a multicenter registry of patients with AMI in Germany.

Results

Of 4902 patients, 509 (10%) did not receive aspirin at the time of discharge from the hospital. The mean follow-up period for these patients was 17 months. Relative contraindications to aspirin were significantly associated with the withholding of aspirin (in-hospital bleeding: odds ratio [OR], 3.56; 95% CI, 1.86-6.80; history of peptic ulcer: OR, 2.49; 95% CI, 1.62-3.83). Absolute contraindications to aspirin were rare (2.2%). Other medications of proven benefit were also given less often in these patients (β-blockers: 49.0% vs 61.9%, P <.001; angiotensin-converting enzyme inhibitors: 65.6% vs 70.2%, P = .06; statins: 12.2% vs 15.1%, P = .10). Patients who were not given aspirin were at high risk for vascular events. They were more likely to have a history of prior AMI (OR, 1.34; 95% CI, 1.02-1.79), were in critical clinical condition at admission more often (cardiogenic shock: OR, 1.98; 95% CI, 1.09-3.56; overt heart failure: OR, 1.6; 95% CI, 1.05-2.3), and received acute revascularization less often (OR, 1.32; 95% CI, 1.05-1.67). The 1-year mortality was 2-times higher in patients who did not receive aspirin than in patients who did receive aspirin (16.5% vs 8.3%, P <.001). A significant association of withheld aspirin at discharge with a higher long-term mortality rate was confirmed with multivariate analysis (OR, 1.62; 95% CI, 1.15-2.29).

Conclusions

Ten percent of patients who sustained an AMI did not receive aspirin at the time of hospital discharge. Most of these patients were at high risk for cardiovascular events. Withheld aspirin was significantly associated with higher mortality rate during follow up.     

Biomarkers to predict recurrent cardiovascular disease: the Heart and Soul Study

Purpose

The study purpose was to evaluate the ability of 6 biomarkers to improve the prediction of cardiovascular events among persons with established coronary artery disease.

Background

Cardiovascular risk algorithms are designed to predict the initial onset of coronary artery disease but are less effective in persons with preexisting coronary artery disease.

Methods

We examined the association of N-terminal prohormone brain natriuretic peptide (Nt-proBNP), cystatin C, albuminuria, C-reactive protein (CRP), interleukin-6, and fibrinogen with cardiovascular events in 979 Heart and Soul Study participants with coronary artery disease after adjusting for demographic, lifestyle, and behavior variables; cardiovascular risk factors; cardiovascular disease severity; medication use; and left ventricular ejection fraction. The outcome was a composite of stroke, myocardial infarction, and coronary heart disease death during an average of 3.5 years of follow-up.

Results

During follow-up, 142 participants (15%) developed cardiovascular events. The highest quartiles (vs lower 3 quartiles) of 5 biomarkers were individually associated with cardiovascular risk after multivariate analysis: Nt-proBNP hazard ratio (HR) = 2.13 (95% confidence interval [CI], 1.43-3.18); cystatin C HR = 1.72 (95% CI, 1.10-2.70); albuminuria HR = 1.71 (95% CI, 1.15-2.54); CRP HR = 2.00 (95% CI, 1.40-2.85); and interleukin-6 HR = 1.76 (95% CI, 1.22-2.53). When all biomarkers were included in the multivariable analysis, only Nt-proBNP, albuminuria, and CRP remained significant predictors of events: HR = 1.88 (95% CI, 1.23-2.85), HR = 1.63 (95% CI, 1.09-2.43), and HR = 1.82 (95% CI, 1.24-2.67), respectively. The area under the receiver operator curve for clinical predictors alone was 0.73 (95% CI, 0.68-0.78); adding Nt-proBNP, albuminuria, and CRP significantly increased the area under the receiver operator curve to 0.77 (95% CI, 0.73-0.82, P <.005).

Conclusion

Among persons with prevalent coronary artery disease, biomarkers reflecting hemodynamic stress, kidney damage, and inflammation added significant risk discrimination for cardiovascular events.     

Complete versus culprit vessel percutaneous coronary intervention in multivessel disease: a randomized comparison

Background

The purpose of this study was to compare the safety, efficacy, and costs of complete versus “culprit” vessel revascularization in multivessel coronary artery disease treated with percutaneous coronary interventions (PCI).

Methods

Patients with multivessel disease and an identified culprit vessel were randomly assigned to complete revascularization of vessels ≥50% stenoses (n = 108) versus revascularization limited to the culprit vessel (n = 111). The primary end point, major adverse cardiac events (MACE), were defined as cardiac or noncardiac death, myocardial infarction, need for coronary artery bypass graft surgery, and repeat PCI up to 1 year.

Results

Despite equal MACE at 24 hours (6.3% vs 7.4%), strategy success was higher in the culprit vessel than in the complete revascularization group (93.7% vs 81.5%, P = .007). MACE rates at 1 month (14.4% vs 9.3%), 1 year (32.4% vs 26.9%), and 4.6 ± 1.2 years (40.4% vs 34.6%) were similar in both groups. Repeat PCI was performed more often in the culprit vessel group (31.2% vs 21.2%, P = .06). A lower consumption of medical material was associated with lower procedural costs in the culprit vessel group (5784 vs 7315 Euros; P < .001). However, between 1 year and the end of follow-up, costs had equalized in both groups.

Conclusions

Complete versus culprit vessel revascularization in multivessel coronary disease treated with PCI was associated with a lower strategy success rate, similar MACE rates, and initially higher costs. However, over the long term, more repeat PCIs were conducted in patients treated by culprit revascularization only, mostly because of the need to treat lesions initially left untreated. As a consequence, incremental costs had equalized within 1 year. The decision of whether to perform culprit vessel or complete revascularization can be made on an individual basis.     

Early sustained ventricular arrhythmias complicating acute myocardial infarction

Objective

Sustained ventricular arrhythmias complicate 2% to 20% of acute myocardial infarctions (MIs) and are associated with increased in-hospital mortality. However, it remains unclear whether successful mechanical revascularization improves outcomes in these patients. The objective of this analysis was to identify predictors of sustained ventricular arrhythmias after acute MI and to determine the influence of successful revascularization on in-hospital mortality.

Methods

We conducted a retrospective cohort study of all patients who underwent percutaneous coronary intervention for acute MI in New York State between 1997 and 1999.

Results

Of the 9015 patients who underwent percutaneous coronary intervention for acute MI, 472 (5.2%) developed sustained ventricular tachycardia (VT) or ventricular fibrillation (VF) before revascularization. After multivariable adjustment, independent predictors of sustained VT/VF included cardiogenic shock (odds ratio [OR], 4.10; 95% confidence interval [CI], 3.20-5.58; P <.001), heart failure (OR, 2.86; 95% CI, 2.24-3.67: P <.001), chronic kidney disease (OR, 2.58; 95% CI, 1.27-5.23; P = .009), and presentation within 6 hours of symptom onset (OR, 1.46; 95% CI, 1.18-1.81; P = .001). Patients with sustained VT/VF had greater in-hospital mortality (16.3% vs 3.7%, P <.001). Although successful percutaneous coronary intervention was associated with decreased in-hospital mortality in patients with VT/VF (P <.001), patients with sustained VT/VF and successful revascularization experienced increased mortality compared with patients without sustained ventricular arrhythmias (P <.001).

Conclusion

Among patients undergoing percutaneous coronary intervention for acute MI, sustained VT/VF remains a significant complication associated with a 4-fold increased risk of in-hospital mortality. Early mortality is reduced after successful percutaneous coronary intervention, but remains elevated in this high-risk group.     

Serologic markers of persistent Chlamydia pneumonia infection and long-term prognosis after successful coronary stenting

Background

Previous studies have shown an incremental role of inflammation in late prognosis following coronary stenting (CS). In particular, high preprocedural levels of plasma C-reactive protein (CRP) have been related to increased hazard of late ischemic complications. Persistent Chlamydia pneumoniae (Cp) infection, detected by positive IgA anti-Cp titers, may be associated with this inflammatory process and portend a high risk of late adverse prognosis after CS.

Methods

A total of 483 consecutive patients with either stable or unstable coronary syndromes were followed-up for 1 year after successful CS. The composite of cardiac death, myocardial infarction, rehospitalization for rest-unstable angina, and exertional angina, whichever occurred first, was the clinical end point. Additionally, the rate of in-stent restenosis and progression of coronary artery disease during this period were evaluated. Anti-Cp titers and plasma CRP levels were measured before the procedure.

Results

Positive immunoglobulin A (IgA), but not positive immunoglobulin G (IgG), titers were significantly associated with high plasma CRP levels in patients with unstable coronary syndromes (P = .005), but not in those with stable angina (P = .7). Moreover, positive IgA titers were significantly related to increased risk of both the composite clinical end point (P = .04) and progression of coronary artery disease (P < .001) in patients with unstable coronary syndromes but not in those with stable angina. Neither positive IgA nor positive IgG titers were associated with the rate of in-stent restenosis.

Conclusions

Persistent Cp infection may drive an inflammatory response in the coronary vasculature and portends an adverse late outcome after CS in patients with unstable coronary syndromes.