Comparison of temporal changes in established cardiovascular biomarkers after acute coronary syndrome between Caucasian and Chinese patients with diabetes mellitus.

Background: Population means of conventional cardiovascular biomarkers are known to differ between ethnic groups. In this study we performed detailed comparisons in the temporal pattern of these biomarkers between Caucasian and Chinese diabetic patients with acute coronary syndrome (ACS).Methods: We studied differences in temporal changes of established cardiovascular biomarkers, including high-density lipoprotein (HDL), low-density lipoprotein (LDL), total cholesterol, cardiac Troponin T (TnT), NT-proBNP and C-reactive protein (CRP), in 48 Chinese and 48 clinically matched Caucasian patients with type 2 diabetes mellitus who were admitted for ACS. Blood samples were collected at regular time intervals during 30 days to 1 year after the index ACS.Results: In the >30 day post ACS period, mean serum levels of LDL (2.16 vs. 1.47 mmol/L; p-value <0.001), total cholesterol (4.08 vs. 3.11 mmol/L; p-value <0.001), TnT (11.0 vs. 7.76 ng/L; p-value 0.010) and CRP (2.0 vs. 0.78 mg/L; p-value <0.001) were systematically higher in Caucasian than in Chinese patients. HDL and NT-proBNP levels were similar.Conclusions: Our study showed clinically relevant differences in levels of established cardiovascular biomarkers between Caucasian and Chinese post ACS patients. Further cross-ethnic studies are warranted to determine secondary prevention treatment biomarker targets in specific populations.

Decline in 20-year mortality after myocardial infarction in patients with chronic kidney disease: evolution from the prethrombolysis to the percutaneous coronary intervention era.

Cardiovascular disease is the main cause of death in patients with chronic kidney disease (CKD). Here we measured temporal trends in treatment and mortality after myocardial infarction (MI) depending on kidney function at presentation in 12,087 patients admitted for MI to a coronary care unit from 1985 to 2008. The patients were categorized into those with normal kidney function (estimated glomerular filtration rate over 90 ml/min per 1.73 m(2)), and those with CKD as defined by Kidney Foundation practice guidelines, with 8632 patients (71%) at CKD stages 2-5. Use of evidence-based care increased over time in all CKD stages. Mortality rates fell over the entire time period. When comparing data from 2000-2008 to that from 1985-1990, adjusted 30-day mortality fell both in patients with CKD stages 4-5 (adjusted odds 0.33, 95% confidence interval 0.18-0.60) and in those without kidney impairment (adjusted odds 0.21, 95% confidence interval 0.10-0.42). This mortality decrease was sustained during long-term follow-up. There was no significant interaction between kidney function and decade of admission. Overall, median survival was over 20, 15, 8, and 1.8 years for patients with normal kidney function, stage 2, stage 3, and stage 4-5 CKD, respectively. Thus, during the past 25 years, treatment of patients with a MI improved substantially with a concomitant decline in mortality. Although our findings were similar for all stages of kidney function, the prognosis remains poor for patients with stage 4-5 CKD.

Potential role of left atrial strain in estimation of left atrial pressure in patients with chronic heart failure.

AIMS: In a large proportion of heart failure with reduced ejection fraction (HFrEF) patients, echocardiographic estimation of left atrial pressure (LAP) is not possible when the ratio of the peak early left ventricular filling velocity over the late filling velocity (E/A ratio) is not available, which may occur due to several potential causes. Left atrial reservoir strain (LASr) is correlated with LV filling pressures and may serve as an alternative parameter in these patients. The aim of this study was to determine whether LASr can be used to estimate LAP in HFrEF patients in whom E/A ratio is not available. METHODS AND RESULTS: Echocardiograms of chronic HFrEF patients were analysed and LASr was assessed with speckle tracking echocardiography. LAP was estimated using the current ASE/EACVI algorithm. Patients were divided into those in whom LAP could be estimated using this algorithm (LAPe) and into those in whom this was not possible because E/A ratio was not available (LAPne). We assessed the prognostic value of LASr on the primary endpoint (PEP), which comprised the composite of hospitalization for the management of acute or worsened HF, left ventricular assist device implantation, cardiac transplantation, and cardiovascular death, whichever occurred first in time. We studied 153 patients with a mean age of 58 years of whom 76% men and 82% who were in NYHA class I-II. A total of 86 were in the LAPe group and 67 in the LAPne group. LASr was significantly lower in the LAPne group as compared with the LAPe group (15.8% vs. 23.8%, P < 0.001). PEP-free survival at a median follow-up of 2.5 years was 78% in LAPe versus 51% in LAPne patients. An increase in LASr was significantly associated with a reduced risk of the PEP in LAPne patients (adjusted hazard ratio: 0.91 per %, 95% confidence interval 0.84-0.98). An abnormal LASr (<18%) was associated with a five-fold increase in reaching the PEP. CONCLUSIONS: In HFrEF patients in whom echocardiographic estimation of LAP is not possible due to due to unavailability of E/A ratio, assessing LASr potentially carries added clinical and prognostic value.

Persistent peripheral and microcirculatory perfusion alterations after out-of-hospital cardiac arrest are associated with poor survival.

OBJECTIVE: To evaluate sublingual microcirculatory and peripheral tissue perfusion parameters in relation to systemic hemodynamics during and after therapeutic hypothermia following out-of-hospital cardiac arrest. DESIGN: Prospective observational study. SETTING: Intensive cardiac care unit at a university teaching hospital. SUBJECTS: We followed 80 patients, of whom 25 were included after out-of-hospital cardiac arrest. INTERVENTION: In all patients, we induced therapeutic hypothermia to 33°C during the first 24 hrs of admission. MEASUREMENTS AND MAIN RESULTS: Complete hemodynamic measurements were obtained directly on intensive cardiac care unit admission (baseline), during induced hypothermia (T1), directly after rewarming (T2), and another 24 hrs later (T3). In addition, the sublingual microcirculation was observed using sidestream dark-field imaging, and peripheral tissue perfusion was monitored with the peripheral perfusion index, capillary refill time, tissue oxygen saturation, and forearm-to-fingertip skin temperature gradient. During hypothermia, all sublingual microcirculatory parameters decreased significantly together with peripheral capillary refill time and the peripheral perfusion index, followed by a significant increase at T2. Changes in sublingual and peripheral tissue perfusion parameters were significantly related to changes in central body temperature, but not to changes in systemic hemodynamic variables such as cardiac index or mean arterial pressure. Surprisingly, these parameters were significantly lower in nonsurvivors (n=6) at admission and after rewarming. Persistent alterations in these parameters were related with the prevalence of organ dysfunction and were highly predictive of mortality. CONCLUSIONS: Following out-of-hospital cardiac arrest, the early postresuscitation phase is characterized by abnormalities in sublingual microcirculation and peripheral tissue perfusion, which are caused by vasoconstriction due to induced systemic hypothermia and not by impaired systemic blood flow. Persistence of these alterations is associated with organ failure and death, independent of systemic hemodynamics.

SYNTAX score in relation to intravascular ultrasound and near-infrared spectroscopy for the assessment of atherosclerotic burden in patients with coronary artery disease.

AIMS: The aim of this study was to examine the relationship between the anatomical SYNTAX score (SXscore), derived from all three coronary arteries, and coronary wall pathology measured by radiofrequency intravascular ultrasound (RF-IVUS) and near-infrared spectroscopy (NIRS) in a single non-culprit segment. METHODS AND RESULTS: In patients referred for coronary angiography (N=88) or PCI (N=592) for stable angina or acute coronary syndrome, the SYNTAX score calculator (www.syntaxscore.com) was used to determine the SXscore before PCI, if applicable. RF-IVUS and/or NIRS were performed in a non-stenotic 40 mm study segment following the clinically indicated angiography/PCI. After adjustment for multiple confounders, a higher SXscore was associated with higher segmental plaque volume in the study segment (2.21 mm3 per SXscore point, 95% CI: 0.92-3.50, p-value 0.001), as well as with higher volume of fibrous (0.93 mm3 per point) and fibro-fatty tissue (0.29 mm3 per point). A higher SXscore was also associated with a higher NIRS-derived lipid core burden index (LCBI) in the full study segment (1.35 units per SXscore point, 95% CI: 0.22-2.47, p-value 0.019). Importantly, SXscore correlated with the fatty/fibro-fatty and LCBI signals despite adjusting for plaque burden. CONCLUSIONS: In patients with CAD, higher SXscores are associated with higher atherosclerotic burden as assessed by RF-IVUS and NIRS in a single non-stenotic coronary artery segment.

Adiponectin in Relation to Coronary Plaque Characteristics on Radiofrequency Intravascular Ultrasound and Cardiovascular Outcome.

BACKGROUND: Prospective data on the associations of adiponectin with in-vivo measurements of degree, phenotype and vulnerability of coronary atherosclerosis are currently lacking. OBJECTIVE: To investigate the association of plasma adiponectin with virtual histology intravascular ultrasound (VH-IVUS)-derived measures of atherosclerosis and with major adverse cardiac events (MACE) in patients with established coronary artery disease. METHODS: In 2008-2011, VH-IVUS of a non-culprit non-stenotic coronary segment was performed in 581 patients undergoing coronary angiography for acute coronary syndrome (ACS, n = 318) or stable angina pectoris (SAP, n = 263) from the atherosclerosis-intravascular ultrasound (ATHEROREMO-IVUS) study. Blood was sampled prior to coronary angiography. Coronary plaque burden, tissue composition, high-risk lesions, including VH-IVUS-derived thin-cap fibroatheroma (TCFA), were assessed. All-cause mortality, ACS, unplanned coronary revascularization were registered during a 1-year-follow-up. All statistical tests were two-tailed and p-values < 0.05 were considered statistically significant. RESULTS: In the full cohort, adiponectin levels were not associated with plaque burden, nor with the various VH-tissue types. In SAP patients, adiponectin levels (median[IQR]: 2.9(1.9-3.9) µg/mL) were positively associated with VH-IVUS derived TCFA lesions, (OR[95%CI]: 1.78[1.06-3.00], p = 0.030), and inversely associated with lesions with minimal luminal area (MLA) ≤ 4.0 mm2 (OR[95%CI]: 0.55[0.32-0.92], p = 0.025). In ACS patients, adiponectin levels (median[IQR]: 2.9 [1.8-4.1] µg/mL)were not associated with plaque burden, nor with tissue components. Positive association of adiponectin with death was present in the full cohort (HR[95%CI]: 2.52[1.02-6.23], p = 0.045) and (borderline) in SAP patients (HR[95%CI]: 8.48[0.92-78.0], p = 0.058). In ACS patients, this association lost statistical significance after multivariable adjustment (HR[95%CI]: 1.87[0.67-5.19], p = 0.23). CONCLUSION: In the full cohort, adiponectin levels were associated with death but not with VH-IVUS atherosclerosis measures. In SAP patients, adiponectin levels were associated with VH-IVUS-derived TCFA lesions. Altogether, substantial role for adiponectin in plaque vulnerability remains unconfirmed.

Temporal trends in long-term mortality of patients with acute heart failure: Data from 1985-2008.

BACKGROUND: Heart failure (HF) has a poor prognosis. Patients with acute heart failure in particular have a high risk of dying. However, there is a lack of data regarding their long-term mortality and changes there-in with time. The aim of our study was to describe trends in short- and long-term mortality of patients hospitalized with acute HF in the period from 1985 through 2008. In addition, we determined the prognostic worth of the aetiology of HF. METHODS AND RESULTS: We included a consecutive series of 1810 patients with acute HF in this prospective registry in the period of 1985 through 2008. The cumulative one-year mortality rate of the patients was 35%. The short-term prognosis remained unchanged over the decades. However, the cumulative mortality rate ten years after admission was lowest in the last decade (73% in 2000-2008 vs. 78% in 1985-1999, p=0.001). After multivariable adjustment, the ten-year mortality rate was lower in the last decade as compared to the first decade (hazard ratio (HR) 0.83; 95% confidence interval (CI) 0.71-0.96). Ischemic cardiomyopathy was associated with a higher mortality (HR 1.32; 95% CI 1.12-1.54) when compared to other causes of HF. CONCLUSIONS: Patients admitted with acute HF were found to have both high short-term and long-term mortality. Long-term prognostic improvement in the last decade was observed among patients with a reduced ejection fraction. While patients with HF due to valvular heart disease had the best prognosis, an ischemic aetiology of HF was associated with the worst outcome.

Repeated measurements of NT-pro-B-type natriuretic peptide, troponin T or C-reactive protein do not predict future allograft rejection in heart transplant recipients.

BACKGROUND: Studies on the prognostic value of serial biomarker assays for future occurrence of allograft rejection (AR) are scarce. We examined whether repeated measurements of NT-pro-B-type natriuretic peptide (NT-proBNP), troponin T (TropT) and C-reactive protein (CRP) predict AR. METHODS: From 2005 to 2010, 77 consecutive heart transplantation (HTx) recipients were included. The NT-proBNP, TropT, and CRP were measured at 16 ± 4 (mean ± standard deviation) consecutive routine endomyocardial biopsy surveillance visits during the first year of follow-up. Allograft rejection was defined as International Society for Heart and Lung Transplantation (ISHLT) grade 2R or higher at endomyocardial biopsy. Joint modeling was used to assess the association between repeated biomarker measurements and occurrence of future AR. Joint modeling accounts for dependence among repeated observations in individual patients. RESULTS: The mean age of the patients at HTx was 49 ± 9.2 years, and 68% were men. During the first year of follow-up, 1,136 biopsies and concurrent blood samples were obtained, and 56 patients (73%) experienced at least one episode of AR. All biomarkers were elevated directly after HTx and achieved steady-state after ∼ 12 weeks, both in patients with or without AR. No associations were present between the repeated measurements of NT-proBNP, TropT, or CRP and AR both early (weeks 0-12) and late (weeks 13-52) in the course after HTx (hazard ratios for weeks 13-52: 0.96 (95% confidence interval, 0.55-1.68), 0.67 (0.27-1.69), and 1.44 (0.90-2.30), respectively, per ln[unit]). Combining the three biomarkers in one model also rendered null results. CONCLUSION: The temporal evolution of NT-proBNP, TropT, and CRP before AR did not predict occurrence of acute AR both in the early and late course of the first year after HTx.

Impact of renin-angiotensin system inhibitors on mortality and major cardiovascular endpoints in hypertension: A number-needed-to-treat analysis.

OBJECTIVE: To assess the effectiveness of renin-angiotensin aldosterone system (RAAS) inhibitors to prevent all-cause and cardiovascular death, myocardial infarction and stroke in hypertensive patients considering the number needed to treat (NNT). METHODS: Data from a meta-analysis of 18 prospective, randomized, controlled morbidity-mortality trials (68 343 RAAS inhibitor; 84 543 control) were used to calculate NNTs for the prevention of all-cause and cardiovascular mortality, myocardial infarction, and stroke. RESULTS: Angiotensin-converting enzyme (ACE) inhibitors were used in 7 trials and angiotensin receptor blockers (ARBs) in 11 trials. Mean follow-up was 4.3years. The annual incidence rate of all-cause mortality was 0.0233 in patients randomized to RAAS inhibitors versus 0.0252 in controls (hazard ratio 0.95, 95% confidence interval 0.91 to 0.99). The corresponding median NNT to prevent one death was 113 (2.5-97.5th percentile, 85 to 168) in favor of RAAS inhibitors, which was driven by ACE inhibitors (NNT 67, 2.5-97.5th percentile, 53 to 92) rather than ARBs (NNT 335, 2.5-97.5th percentile, -4341 to 5076). Results for cardiovascular mortality (NNT 116 for ACE inhibitors and 409 for ARBs, respectively) and myocardial infarction (NNT 80 and 338, respectively) also appeared to be driven by ACE inhibitors. We found a lower NNT for stroke in favor of ARB (NNT 337 and 131, respectively) although this difference was statistically non-significant. CONCLUSION: Among hypertensive patients, ACE inhibitors but not ARBs, substantially reduce all-cause and cardiovascular mortality and myocardial infarction.

Systematic adjudication of myocardial infarction end-points in an international clinical trial.

BACKGROUND: Clinical events committees (CEC) are used routinely to adjudicate suspected end-points in cardiovascular trials, but little information has been published about the various processes used. We reviewed results of the CEC process used to identify and adjudicate suspected end-point (post-enrolment) myocardial infarction (MI) in the large Platelet Glycoprotein IIb/IIIa in Unstable Angina: Receptor Suppression Using Integrilin (Eptifibatide) Therapy (PURSUIT) trial. METHODS: The PURSUIT trial randomised 10,948 patients with acute coronary syndromes to receive eptifibatide or placebo. A central adjudication process was established prospectively to identify all suspected MIs and adjudicate events based on protocol definitions of MI. Suspected MIs were identified by systematic review of data collection forms, cardiac enzyme results, and electrocardiograms. Two physicians independently reviewed all suspected events. If they disagreed whether a MI had occurred, a committee of cardiologists adjudicated the case. RESULTS: The CEC identified 5005 patients with suspected infarction (46%), of which 1415 (28%) were adjudicated as end-point infarctions. As expected, the process identified more end-point events than did the site investigators. Absolute and relative treatment effects of eptifibatide were smaller when using CEC-determined MI rates rather than site investigator-determined rates. The site-investigator reporting of MI and the CEC assessment of MI disagreed in 20% of the cases reviewed by the CEC. CONCLUSIONS: End-point adjudication by a CEC is important, to provide standardised, systematic, independent, and unbiased assessment of end-points, particularly in trials that span geographic regions and clinical practice settings. Understanding the CEC process used is important in the interpretation of trial results and event rates.

Disagreements between central clinical events committee and site investigator assessments of myocardial infarction endpoints in an international clinical trial: review of the PURSUIT study.

BACKGROUND: Limited information has been published regarding how specific processes for event adjudication can affect event rates in trials. We reviewed nonfatal myocardial infarctions (MIs) reported by site investigators in the international Platelet Glycoprotein IIb/IIIa in Unstable Angina: Receptor Suppression Using Integrilin (Eptifibatide) Therapy (PURSUIT) trial and those adjudicated by a central clinical events committee (CEC) to determine the reasons for differences in event rates. METHODS: The PURSUIT trial randomised 10,948 patients with acute coronary syndromes to receive eptifibatide or placebo. The primary end-point was death or post-enrolment MI at 30 days as assessed by the CEC; this end-point was also constructed using site-reported events. The CEC identified suspected MIs by systematic review of clinical, cardiac enzyme, and electrocardiographic data. RESULTS: The CEC identified 5005 (46%) suspected events, of which 1415 (28%) were adjudicated as MI. The site investigator and CEC assessments of whether a MI had occurred disagreed in 983 (20%) of the 5005 patients with suspected MI, mostly reflecting site misclassification of post-enrolment MIs (as enrolment MIs) or underreported periprocedural MIs. Patients for whom the CEC and site investigator agreed that no end-point MI had occurred had the lowest mortality at 30 days and between 30 days and 6 months, and those with agreement that a MI had occurred had the highest mortality. CONCLUSION: CEC adjudication provides a standard, systematic, independent, and unbiased assessment of end-points, particularly for trials that span geographic regions and clinical practice settings. Understanding the review process and reasons for disagreement between CEC and site investigator assessments of MI is important to design future trials and interpret event rates between trials.

Relation of admission glucose levels, short- and long-term (20-year) mortality after acute myocardial infarction.

We examined temporal trends in mortality after myocardial infarction from 1985 to 2008 depending on admission glucose levels. We included 11,324 consecutive patients admitted to our intensive coronary care unit for myocardial infarction from 1985 to 2008. Patients were categorized into normal, mild, and severe hyperglycemia groups (admission glucose levels <140, 140 to 200, and ≥200 mg/dl, respectively). Temporal trends were determined using 3 groups: 1985 to 1990, 1990 to 2000, and 2000 to 2008. The prevalence of hyperglycemia increased from 26% in the 1980s to 49% in the 2000s. The prevalence of hyperglycemia primarily increased in patients without diabetes. Kaplan-Meier mortality was 4%, 8%, and 17% at 30 days and 64%, 71%, and 82% at 20 years in patients with normal, mild, and severe hyperglycemia, respectively. Compared with normal admission glucose level, adjusted 30-day mortality was 3.6-fold greater (95% confidence interval 2.9 to 4.3) in patients with severe hyperglycemia. This association was not dependent on diabetic status (p for interaction = 0.43) but was dependent on the decade of hospitalization with a stronger association from 2000 to 2008 (adjusted odds ratio 7.7, 95% confidence interval 5.4 to 11, p for interaction <0.001). Compared with diabetes, hyperglycemia was a better discriminator for 30-day mortality. Mortality at 30 days decreased from 1985 to 2008, however, it decreased less in patients with hyperglycemia compared with those with normoglycemia. In conclusion, elevated admission glucose levels are common in patients with myocardial infarction and are strongly associated with increased mortality. Mortality decreased less from 1985 to 2008 in patients with hyperglycemia compared with those with normoglycemia. Efforts that establish optimal treatment for these patients remain warranted.

Adiponectin in Relation to Coronary Plaque Characteristics on Radiofrequency Intravascular Ultrasound and Cardiovascular Outcome / Relação da Adiponectina com as Características da Placa Aterosclerótica ao Ultrassom Intravascular com Radiofrequência e Desfechos Cardiovasculares

Abstract Background: Prospective data on the associations of adiponectin with in-vivo measurements of degree, phenotype and vulnerability of coronary atherosclerosis are currently lacking. Objective: To investigate the association of plasma adiponectin with virtual histology intravascular ultrasound (VH-IVUS)-derived measures of atherosclerosis and with major adverse cardiac events (MACE) in patients with established coronary artery disease. Methods: In 2008-2011, VH-IVUS of a non-culprit non-stenotic coronary segment was performed in 581 patients undergoing coronary angiography for acute coronary syndrome (ACS, n = 318) or stable angina pectoris (SAP, n = 263) from the atherosclerosis-intravascular ultrasound (ATHEROREMO-IVUS) study. Blood was sampled prior to coronary angiography. Coronary plaque burden, tissue composition, high-risk lesions, including VH-IVUS-derived thin-cap fibroatheroma (TCFA), were assessed. All-cause mortality, ACS, unplanned coronary revascularization were registered during a 1-year-follow-up. All statistical tests were two-tailed and p-values < 0.05 were considered statistically significant. Results: In the full cohort, adiponectin levels were not associated with plaque burden, nor with the various VH-tissue types. In SAP patients, adiponectin levels (median[IQR]: 2.9(1.9-3.9) µg/mL) were positively associated with VH-IVUS derived TCFA lesions, (OR[95%CI]: 1.78[1.06-3.00], p = 0.030), and inversely associated with lesions with minimal luminal area (MLA) ≤ 4.0 mm2 (OR[95%CI]: 0.55[0.32-0.92], p = 0.025). In ACS patients, adiponectin levels (median[IQR]: 2.9 [1.8-4.1] µg/mL)were not associated with plaque burden, nor with tissue components. Positive association of adiponectin with death was present in the full cohort (HR[95%CI]: 2.52[1.02-6.23], p = 0.045) and (borderline) in SAP patients (HR[95%CI]: 8.48[0.92-78.0], p = 0.058). In ACS patients, this association lost statistical significance after multivariable adjustment (HR[95%CI]: 1.87[0.67-5.19], p = 0.23). Conclusion: In the full cohort, adiponectin levels were associated with death but not with VH-IVUS atherosclerosis measures. In SAP patients, adiponectin levels were associated with VH-IVUS-derived TCFA lesions. Altogether, substantial role for adiponectin in plaque vulnerability remains unconfirmed.

Resumo Fundamento: Faltam dados prospectivos sobre as associações de adiponectina com medidas in-vivo de grau, fenótipo e vulnerabilidade da aterosclerose coronariana. Objetivo: Investigar a associação da adiponectina plasmática com medidas de aterosclerose derivadas de ultrassonografia virtual intravascular (VH-IVUS) e eventos cardíacos adversos importantes (major adverse cardiac events - MACE) em pacientes com doença arterial coronariana estabelecida. Métodos: Em 2008-2011, a VH-IVUS de um segmento coronariano não estenótico não culpado foi realizado em 581 pacientes submetidos à angiografia coronariana para síndrome coronariana aguda (SCA, n = 318) ou angina pectoris estável (APE, n = 263) a partir do estudo de ultrassonografia aterosclerótica-intravascular (ATHEROREMO-IVUS). Sangue foi amostrado antes da angiografia coronária. Foram avaliados a carga de placa coronária, a composição tecidual, as lesões de alto risco, incluindo fibroateroma de capa fina (FCF) derivado de VH-IVUS. Mortalidade por todas as causas, SCA, e revascularização coronária não planejada foram registradas durante um ano de acompanhamento. Todos os testes estatísticos foram bicaudais e os valores de p < 0,05 foram considerados estatisticamente significativos. Resultados: Na coorte completa, os níveis de adiponectina não foram associados à carga de placa, nem a vários tipos de tecido virtual histológico. Entre os pacientes com APE, os níveis de adiponectina (mediana[IIQ]: 2,9(1,9-3,9) µg/mL) foram associados positivamente às lesões FCF derivadas de VH-IVUS, (OR[IC 95%]: 1,78[1,06-3,00], p = 0,030), e inversamente associados a lesões com área luminal mínima (ALM) ≤4,0 mm2 (OR[IC 95%]: 0,55[0,32-0,92], p = 0,025). Em pacientes com SCA, os níveis de adiponectina (mediana[IIQ]: 2,9 [1,8-4,1] µg/mL) não foram associados à carga de placa nem a componentes teciduais. A associação positive de adiponectina ao óbito esteve presente na coorte completa (HR[IC 95%]: 2,52[1,02-6,23], p = 0,045) e (limítrofe) em pacientes com APE (HR[IC 95%]: 8,48[0,92-78,0], p = 0,058). Entre pacientes com SCA, essa associação perdeu significância estatística após ajuste multivariado (HR[IC 95%]: 1,87[0,67-5,19], p = 0,23). Conclusão: Na coorte completa, os níveis de adiponectina foram associados à obito, mas não a medidas de aterosclerose por VH-IVUS. Em pacientes com APE, os níveis de adiponectina foram associados a lesões FCF derivadas de VH-IVUS. Em geral, o papel da adiponectina na vulnerabilidade da placa permanece não confirmado.

Changes in clinical profile, treatment, and mortality in patients hospitalised for acute myocardial infarction between 1985 and 2008.

OBJECTIVES: To quantify the impact of the implementation of treatment modalities into clinical practice since 1985, on outcome of patients with ST-segment elevation myocardial infarction (STEMI) or non-ST-segment elevation myocardial infarction (NSTEMI). METHODS: All consecutive patients admitted for STEMI or NSTEMI at the Thoraxcenter between 1985 and 2008 were included. Baseline characteristics, pharmacological and invasive treatment modalities, and survival status were collected. The study population was categorised in three groups of patients: those hospitalised between 1985-1990, 1990-2000, and 2000-2008. RESULTS: We identified 14,434 patients hospitalised for myocardial infarction (MI). Both STEMI and NSTEMI patients were increasingly treated with the current guideline based therapy. In STEMI, at 30 days following admission, cumulative mortality rate decreased from 17% in 1985-1990 to 13% in 1990-2000, and to 6% in 2000-2008. Adjusted 30-day and three-year mortality in the last period was 80% and 68% lower than in 1985, respectively. In NSTEMI, at 30 days following admission, cumulative mortality rate decreased from 6% in 1985-1990 to 4% in 1990-2000, and to 2% in 2000-2008. Adjusted 30-day and three-year mortality in the last period was 78% and 49% lower than in 1985, respectively. For patients admitted between 2000 and 2008, 3 year survival of STEMI and NSTEMI patients was 87% and 88%, respectively. CONCLUSIONS: Our results indicate substantial improvements in acute- and long-term survival in patients hospitalised for MI, related to improved acute- as well as long-term treatment. Early medical evaluation in suspected MI and intensive early hospital treatment both remain warranted in the future.