Conduction abnormalities during dipyridamole stress testing.

Pharmacological stress tests using dipyridamole are considered to be safe. However, cases of atrioventricular (AV) block have been reported. We retrospectively analyzed ECG at baseline and during dipyridamole stress tests of 2010 consecutive patients (patients with second or third degree AV block were excluded). At baseline, 350 (17.4%) patients had conduction abnormalities. Following dipyridamole infusion 16 patients (0.8%) developed a transient change in AV conduction (15 patients) and or sinus arrest (1 patient). Compared to patients without baseline conduction abnormalities, patients with any conduction abnormalities at baseline were at a higher risk for the development of AV block after dipyridamole infusion [0.3% vs 3.14%, respectively; P < .0001].

Real-World Use of Novel P2Y12 Inhibitors in Patients with Acute Myocardial Infarction: A Treatment Paradox.

OBJECTIVE: To assess the real-world use, clinical outcomes, and adherence to novel P2Y12 inhibitors. METHODS: We evaluated 1,093 consecutive acute myocardial infarction patients undergoing a percutaneous intervention. Patients were derived from a prospective, multicenter, nationwide registry and were followed for 30 days; 381 patients (35%) received clopidogrel, 468 (43%) received prasugrel, and 244 (22%) received ticagrelor. Patients treated with clopidogrel were older and more likely to suffer from chronic renal failure and stroke and/or present with non-ST-elevation myocardial infarction (NSTEMI) (p < 0.01 for all). Independent predictors of undertreatment with novel P2Y12 inhibitors included: older age (OR 0.17; 95% CI 0.1-0.27, p < 0.0001), a prior stroke (OR 0.41; 95% CI 0.2-0.68, p = 0.008), and NSTEMI (OR 0.37; 95% CI 0.26-0.54, p < 0.0001). RESULTS: Novel P2Y12 inhibitors were associated with a lower incidence of cardiovascular events, major bleeding, and/or death (7.6 vs.11%, HR 0.67; 95% CI 0.43-1, p = 0.05). However, after a multivariate analysis this trend was not statistically significant. Patients discharged with ticagrelor versus thienopyridines demonstrated a higher rate of crossover to other P2Y12 inhibitors (11 vs. 5%, p = 0.03). CONCLUSIONS: In a real-world cohort, there was an underutilization of novel P2Y12 inhibitors which was more pronounced in higher-risk subsets that might benefit from novel P2Y12 inhibitors at least as much as other patients.

Diagnostic Value of High-Sensitivity Cardiac Troponin-I in Patients After Out-of-Hospital Cardiac Arrest.

Knowing the etiology of cardiac arrest (CA) is important for treatment decisions. Results of previous studies on the diagnostic role of cardiac troponin in patients resuscitated from CA are controversial, few studies were done during the era of high-sensitivity cardiac troponin-I (hs-cTnI), and kinetics of hs-cTnI was not thoroughly investigated. We aimed to explore the diagnostic value of hs-cTnI in patients resuscitated from out-of-hospital CA (OHCA). This retrospective study included 201 consecutive patients after OHCA admitted to the intensive cardiac care unit at Rambam Health Care Campus from 2016 to 2021. Patients were divided into 2 groups according to etiology of CA: group 1-patients with definite acute myocardial infarction (AMI), group 2-patients in whom AMI was excluded. Values of hs-cTnI on admission, peak hs-cTnI, and hs-cTnI upslope were compared between patients with AMI and non-AMI. Peak hs-cTnI and hs-cTnI upslope differed significantly between patients with non-AMI versus AMI CA (median 1,424 vs 32,558 ng/L, p <0.0001 and median 109 vs 2,322 ng/L/h, p <0.0001, respectively). Moreover, peak hs-cTnI and hs-cTnI upslope were found to have good discrimination performance between patients with non-AMI and AMI, with area under the curve receiver operating characteristics (ROC) curves of 0.83 and 0.80, respectively. In conclusion, in patients resuscitated from OHCA values of peak hs-cTnI and hs-cTnI upslope could be helpful in the diagnosis of etiology of CA as adjunct to other diagnostic methods.

Type of Anemia, Chronic Non-cardiovascular Illnesses, and Outcomes of Patients with ST-segment Elevation Myocardial Infarction.

OBJECTIVES: To assess the impact of different types of anemia and of concomitant non-cardiovascular chronic illnesses on outcomes of patients with ST-segment elevation myocardial infarction (STEMI) and baseline anemia admitted to the Intensive Cardiac Care Unit. METHODS: Based on the mean corpuscular volume, anemia was stratified into: microcytic (<80 fL), normocytic (≥80, <96 fL), and macrocytic (≥96 fL). Data on concomitant chronic non-cardiovascular illnesses including malignancies were carefully collected. Endpoints included in-hospital bleeding as well as all-cause mortality at long-term follow-up. RESULTS: Of 1,390 patients with STEMI, 294 patients had baseline anemia (21.2%), in whom normocytic, microcytic, and macrocytic anemia was present in 77.2%, 17.0%, and 5.8% patients, respectively. In-hospital bleeding occurred in 25 (8.5%) of the study population without significant differences between the three groups. At a mean follow-up of 5.5±3.5 years, 104 patients (35.4%) had died. Mortality was the highest in patients with macrocytic anemia, followed by patients with normocytic anemia and microcytic anemia (58.8%, 37.0%, and 20.0%, respectively; P=0.009). Chronic non-cardiovascular condition was identified as an independent predictor of both in-hospital bleeding (odds ratio=2.57, P=0.01) and long-term mortality (hazard ratio [HR] 1.54, P=0.019). Performance of coronary angiography within index hospitalization was associated with lower long-term mortality (HR 0.38, P=0.001). Mean corpuscular volume did not predict either in-hospital bleeding or mortality. CONCLUSIONS: Chronic non-cardiovascular illnesses are highly prevalent among patients with STEMI and baseline anemia, and are strongly associated with higher in-hospital bleeding and long-term mortality. Type of anemia is not related to prognosis post-STEMI.

Incidence of early left ventricular thrombus after acute anterior wall myocardial infarction in the primary coronary intervention era.

BACKGROUND: Rapid reperfusion has been shown to decrease mortality and improve left ventricular (LV) function. Previous studies have reported that LV thrombus (LVT) is a major complication of ST-segment elevation acute anterior wall myocardial infarction (AMI). There are little data on LVT in the current primary percutaneous coronary intervention (PPCI) era. We sought to demonstrate the incidence of LVT after AMI in patients treated with PPCI compared with those treated with thrombolysis or with conservative management. METHODS: In a 6-year period, 642 patients with anterior wall AMI and echocardiography were treated with PPCI (n = 297), thrombolysis (n = 128), or conservative treatment (n = 217). Left ventricular thrombus was defined as an echodense mass adjacent to an abnormally contracting myocardial segment. RESULTS: The rate of LVT among anterior wall AMI was 6.2%. Predictors for LVT were reduced ejection fraction (adjusted relative risk 0.71, 95% CI 0.52-0.96) and severe mitral regurgitation (adjusted relative risk 2.48, 95% CI 1.0-6.44). There was no statistical difference in LVT rate according to treatment: 21 (7.1%) of 297 patients in the PPCI group, 10 (7.8%) of 128 patients in the thrombolytic group, and 9 (4.1%) of 217 patients in the conservative group (P = .28). Those in the thrombolytic group were characterized by shorter duration from symptom onset and were generally also treated with heparin/low-molecular weight heparin. CONCLUSIONS: This is the largest report to evaluate the incidence of LVT formation after AMI. In the current era of rapid reperfusion by PPCI, the rate of thrombus formation is similar to that reported in the past and not different than for patients currently treated conservatively or with thrombolysis.

Impact of red blood cell transfusion on clinical outcomes in patients with acute myocardial infarction.

Divergent views remain regarding the safety of treating anemia with red blood cell (RBC) transfusion in patients with acute coronary syndrome (ACS). We used a prospective database to study effect of RBC transfusion in patients with acute myocardial infarction (MI; n = 2,358). Cox regression models were used to determine the association between RBC transfusion and 6-month outcomes, incorporating transfusion as a time-dependent variable. The models adjusted for baseline variables, propensity for transfusion, and nadir hemoglobin previous to the transfusion. One hundred ninety-two patients (8.1%) received RBC transfusion. Six-month mortality rates were higher in patients receiving transfusion (28.1% vs 11.7%, p <0.0001). The adjusted hazard ratio (HR) for mortality was 1.9 in transfused patients (95% confidence interval [CI] 1.3 to 2.9). Interaction between RBC transfusion and nadir hemoglobin with respect to mortality (p = 0.004) was significant. Stratified analyses showed a protective effect of transfusion in patients with nadir hemoglobin < or=8 g/dL (adjusted HR 0.13, 95% CI 0.03 to 0.65, p = 0.013). By contrast, transfusion was associated with increased mortality in patients with nadir hemoglobin >8 g/dL (adjusted HR 2.2, 95% CI 1.5 to 3.3; p <0.0001). Similar results were obtained for the composite end point of death/MI/heart failure (p for interaction = 0.04). In conclusion, RBC transfusion in patients with acute MI and hemoglobin < or =8 g/dL may be appropriate. The increased mortality observed in transfused patients with nadir hemoglobin above 8 g/dL underscores the clinical difficulty of balancing risks and benefits of RBC transfusion in the setting of ACS.

Identification of the gene causing long QT syndrome in an Israeli family.

BACKGROUND: Long QT syndrome is an inherited cardiac disease, associated with malignant arrhythmias and sudden cardiac death. OBJECTIVES: To map and identify the gene responsible for LQTS in an Israeli family. METHODS: A large family was screened for LQTS after one of them was successfully resuscitated from ventricular fibrillation. The DNA was examined for suspicious loci by whole genome screening and the coding region of the LQT2 gene was sequenced. RESULTS: Nine family members, 6 males and 3 females, age (median and interquartile range) 26 years (13, 46), who were characterized by a unique T wave pattern were diagnosed as carrying the mutant gene. The LQTS-causing gene was mapped to chromosome 7 with the A614V mutation. All of the affected members in the family were correctly identified by electrocardiogram. Corrected QT duration was inversely associated with age in the affected family members and decreased with age. CONCLUSIONS: Careful inspection of the ECG can correctly identify LQTS in some families. Genetic analysis is needed to confirm the diagnosis and enable the correct therapy in this disease.

Long-term effects of brief hypoxia due to cardiac arrest: Hippocampal reductions and memory deficits.

OBJECTIVE: To examine the effects of brief hypoxia (<7 min) due to cardiac arrest on the integrity of the brain and performance on memory and executive functions tasks. METHODS: Patients after out-of-hospital cardiac arrest (CA) (n = 9), who were deemed neurologically intact on discharge, were compared to matched patients with myocardial infarction (MI) (n = 9). A battery of clinical and experimental memory and executive functions neuropsychological tests were administered and MRI scans for all patients were collected. Measures of subcortical and cortical volumes and cortical thickness were obtained using FreeSurfer. Manual segmentations of the hippocampus were also performed. APACHE-II scores were calculated based on metrics collected at admission to ICCU for all patients. RESULTS: Significant differences between the two groups were observed on several verbal memory tests. Both hippocampi were significantly reduced (p < 0.05) in the CA patients, relative to MI patients. Hippocampal subfields segmentation showed significantly reduced presubiculum volumes bilaterally. CA patients had on average 10% reduction in volumes bilaterally across hippocampal subfields. No cortical thickness differences survived correction. Significant correlations were observed in the CA group only between the hippocampal volumes and performance on verbal memory tasks, including recollection. Hippocampal volumes and several memory measures (but not other cognitive domains) were strongly correlated with APACHE-II scores on admission in the CA group, but not in the MI group CONCLUSIONS: Chronic patients with cardiac arrest who were discharged from hospital in "good neurological condition" showed an average of 10% reduction in hippocampal volume bilaterally and significant verbal memory deficits relative to matched controls with myocardial infarction, suggesting even brief hypoxic periods suffice to lead to specific hippocampal damage.

Relation of C-reactive protein and new-onset atrial fibrillation in patients with acute myocardial infarction.

Recent studies have implicated systemic inflammation in the genesis and maintenance of atrial fibrillation (AF). A robust inflammatory response is an integral component of the response to tissue injury during acute myocardial infarction (AMI). However, there is no information concerning the association between inflammation and AF in patients with AMI. We studied 1,209 patients admitted for AMI. C-reactive protein (CRP) was measured by a high-sensitivity assay within 12 to 24 hours after symptom onset. The relation between CRP and new-onset AF occurring during the hospital course and at 1 year was analyzed using multivariable logistic regression and Cox models, respectively. New-onset AF during hospitalization occurred in 6.5%, 10.4%, and 17.1% of patients in the first, second and third CRP tertiles, respectively (p trend <0.0001). In a multivariable logistic regression, adjusting for clinical variables and ejection fraction, compared with patients in the first CRP tertile, the odds ratios for AF were 1.5 (95% confidence interval 0.9 to 2.5, p = 0.15) and 2.0 (95% confidence interval 1.2 to 3.3, p = 0.008) in patients in the second and third CRP tertiles, respectively (p for trend = 0.007). In a Cox multivariate analysis, CRP remained an independent predictor of new-onset AF at 1 year. In conclusion, in a large cohort of patients with AMI, there was a graded positive association between increased CRP and new-onset AF. Inflammation may contribute to the development of AF in the setting of AMI.

Ischemic mitral regurgitation and risk of heart failure after myocardial infarction.

BACKGROUND: The development of ischemic mitral regurgitation (MR) after myocardial infarction may impose hemodynamic load during a period of active left ventricular remodeling and promote heart failure (HF). However, few data are available on the relationship between ischemic MR and the long-term risk for HF. METHODS: We prospectively studied 1190 patients admitted for acute myocardial infarction. Mitral regurgitation was assessed by echocardiography and was considered mild, moderate, and severe when the regurgitant jet area occupied less than 20%, 20% to 40%, and greater than 40% of the left atrial area, respectively. The median duration of follow-up was 24 months (range, 6-48 months). RESULTS: Mild and moderate or severe ischemic MR was present in 39.7% and 6.3% of patients, respectively. After adjusting for ejection fraction and clinical variables (age, sex, Killip class, previous infarction, hypertension, diabetes mellitus, anterior infarction, ST-elevation infarction, and coronary revascularization), compared with patients without MR, the hazard ratios for HF were 2.8 (95% confidence interval [CI], 1.8-4.2; P<.001) and 3.6 (95% CI, 2.0-6.4; P<.001) in patients with mild and moderate or severe ischemic MR, respectively. The adjusted hazard ratios for death were 1.2 (95% CI, 0.8-1.8; P = .43) and 2.0 (95% CI, 1.2-3.4; P = .02) in patients with mild and moderate or severe MR, respectively. CONCLUSIONS: There is a graded independent association between the severity of ischemic MR and the development of HF after myocardial infarction. Even mild ischemic MR is associated with an increase in the risk of HF.

Hyponatremia and long-term mortality in survivors of acute ST-elevation myocardial infarction.

BACKGROUND: Hyponatremia, a marker of neurohormonal activation, is a common electrolyte disorder among patients with acute ST-elevation myocardial infarction. The long-term prognostic value of hyponatremia during the acute phase of infarction is not known. METHODS: We studied 978 patients with acute ST-elevation myocardial infarction and without a history of heart failure who survived the index event. During the hospital stay, sodium levels were obtained on admission and at 24, 48, and 72 hours. The median duration of follow-up after hospital discharge was 31 months (range, 9-61 months). RESULTS: Hyponatremia, defined as a mean serum sodium level less than 136 mEq/L, was present during admission in 108 patients (11.0%). In a multivariable Cox proportional hazards model adjusting for other potential clinical predictors of mortality and for left ventricular ejection fraction, hyponatremia during admission remained an independent predictor of postdischarge death (hazard ratio [HR], 2.0; 95% confidence interval [CI], 1.3-3.2; P = .002). Hyponatremia during admission was also independently associated with postdischarge readmission for heart failure (HR, 1.6; 95% CI, 1.1-2.6; P = .04). When serum sodium level was used as a continuous variable, the adjusted HR for death or heart failure was 1.12 for every 1-mEq/L decrease (95% CI, 1.07-1.18; P<.001). CONCLUSION: Hyponatremia in the early phase of ST-elevation myocardial infarction is a predictor of long-term mortality and admission for heart failure after hospital discharge, independent of other clinical predictors of adverse outcome and left ventricular ejection fraction.

Primary percutaneous coronary intervention after out-of-hospital cardiac arrest: patients and outcomes.

BACKGROUND: The decision to perform primary percutaneous coronary intervention in unconscious patients resuscitated after out-of-hospital cardiac arrest is challenging because of uncertainty regarding the prognosis of recovery of anoxic brain damage and difficulties in interpreting ST segment deviations. In ST elevation myocardial infarction patients after OHCA, primary PCI is generally considered the only option for reperfusion. There are few published studies and no randomized trial has yet been performed in this specific group of patients. OBJECTIVES: To define the demographic, clinical and angiographic characteristics, and the prognosis of STEMI patients undergoing primary PCI after out-of-hospital cardiac arrest. METHODS: We performed a retrospective analysis of medical records and used the prospectively acquired information from the Rambam Primary Angioplasty Registry (PARR) and the Rambam Intensive Cardiac Care (RICCa) databases. RESULTS: During the period March 1998 to June 2006, 25 STEMI patients (21 men and 4 women, mean age 56 +/- 11years) after OHCA were treated with primary PCI. The location of myocardial infarction was anterior in 13 patients (52%) and non-anterior in 12 (48%). Cardiac arrest was witnessed in 23 patients (92%), but bystander resuscitation was performed in only 2 patients (8%). Eighteen patients (72%) were unconscious on admission, and Glasgow Coma Scale > 5 was noted in 2 patients (8%). Cardiogenic shock on admission was diagnosed in 4 patients (16%). PCI procedure was successful in 22 patients (88%). In-hospital, 30 day, 6 month and 1 year survival was 76%, 76%, 76% and 72%, respectively. In-hospital, 30 day, 6 month and 1 year survival without severe neurological disability was 68%, 68%, 68% and 64%, respectively. CONCLUSIONS: In a selected group of STEMI patients after out-of-hospital cardiac arrest, primary PCI can be performed with a high success rate and provides reasonably good results in terms of short and longer term survival.

Acute Kidney Injury After Primary Angioplasty: Is Contrast-Induced Nephropathy the Culprit?

BACKGROUND: Acute kidney injury (AKI) following primary percutaneous coronary intervention (pPCI) is frequently interpreted as contrast-induced AKI but may result from other insults. We aimed to determine the causal association of contrast material exposure and the incidence of AKI following pPCI using a control group of propensity score-matched patients with ST-segment-elevation myocardial infarction who were not exposed to contrast material. METHODS AND RESULTS: We studied 2025 patients with ST-segment-elevation myocardial infarction who underwent pPCI and 1025 patients receiving fibrinolysis or no reperfusion who were not exposed to contrast material during the first 72 hours of hospital stay (control group). AKI was defined as creatinine of ≥0.5 mg/dL or >25% rise within 72 hours. AKI rates were similar in the pPCI and control groups (10.3% versus 12.1%, respectively; P=0.38). Propensity score matching resulted in 931 matched pairs with PCI and no PCI, with balanced baseline covariates (standardized difference <0.1). Among propensity score-matched patients, AKI rates were not significantly different with and without PCI (8.6% versus 10.9%, P=0.12). In the pPCI cohort, independent predictors of AKI included age ≥70 years, insulin-treated diabetes mellitus, diuretic therapy, anterior infarction, baseline estimated glomerular filtration rate, and variables related to the presence of pump failure (higher Killip class, intra-aortic balloon pump use) and reduced left ventricular ejection fraction but not contrast material dose. A risk score based on the PCI cohort had similar discriminatory capacity for AKI in the control group (C statistic 0.81±0.02 and 0.78±0.02, respectively; P=0.26). CONCLUSIONS: The development of AKI in patients with ST-segment-elevation myocardial infarction undergoing pPCI is mainly related to older age, baseline estimated glomerular filtration rate, heart failure, and hemodynamic instability. Risk for AKI is similar among ST-segment-elevation myocardial infarction patients with and without contrast material exposure.

Fasting glucose is an important independent risk factor for 30-day mortality in patients with acute myocardial infarction: a prospective study.

BACKGROUND: Stress hyperglycemia in patients with acute myocardial infarction has been associated with increased mortality. Most studies looked at the relationship between admission glucose (AG) and outcome; limited information is available about the clinical significance of fasting glucose (FG). METHODS AND RESULTS: We prospectively studied the relationship between FG and 30-day mortality in 735 nondiabetic patients with acute myocardial infarction. FG (> or =8-hour fast within 24 hours of admission) and AG were measured in each patient. At 30 days, 9 deaths (2%) occurred in patients with normal FG, and 11 (10%), 14 (13%), and 31 (29%) deaths occurred in the first, second, and third tertiles of elevated FG, respectively. Compared with normal FG (<110 mg/dL), the adjusted OR for 30-day mortality progressively increased with higher tertiles of elevated FG (first tertile, 4.6; 95% CI, 1.7 to 12.7; P=0.003; second tertile, 6.4; 95% CI, 2.5 to 16.6; P<0.0001; third tertile, 11.5; 95% CI, 4.7 to 20.0; P<0.0001). Compared with patients categorized as having normal AG (<140 mg/d), the adjusted ORs for tertiles of elevated AG were as follows: first tertile, 1.4 (95% CI, 0.5 to 3.8; P=0.54); second tertile, 3.0 (95% CI, 1.3 to 7.0; P=0.01); and third tertile, 4.4 (95% CI, 2.0 to 9.7; P<0.0001). Compared with patients with normal FG and AG, the adjusted ORs for 30-day mortality were 0.71 (95% CI, 0.15 to 3.4; P=0.67) in patients with elevated AG and normal FG, 3.4 (95% CI, 1.1 to 10.4; P=0.03) for patients with normal AG glucose and elevated FG, and 9.6 (95% CI, 3.5 to 26.0; P<0.0001) for patients with both elevated FG and AG. Comparing nested models showed that including AG failed to improve the prediction of the model based on FG (chi2=5.4, 3 df, P=0.15). In contrast, the addition of FG classes to the model based on AG improved model prediction (chi2=22.4, 3 df, P<0.0001). CONCLUSIONS: There is a graded relation between elevated FG and AG and 30-day mortality in patients with acute myocardial infarction. FG is superior to AG in the assessment of short-term risk.

Haptoglobin polymorphism predicts 30-day mortality and heart failure in patients with diabetes and acute myocardial infarction.

Patients with diabetes presenting with acute myocardial infarction (AMI) have an increased rate of death and heart failure. Patients with diabetes homozygous for the haptoglobin (Hp) 1 allele (Hp 1-1) develop fewer vascular complications. We tested the hypothesis that Hp type is related to the outcome of patients with diabetes presenting with AMI. We prospectively assessed the relationship between Hp type and 30-day mortality and heart failure in 1,437 patients with AMI (506 with diabetes). Multivariate logistic regression identified a significant interaction between Hp type and diabetes status on these outcome measures. Hp type was not related to outcome among patients without diabetes. In contrast, Hp 1-1 was associated with a strong protective effect with regard to the primary end point of death (OR 0.14, P = 0.015) and for death and heart failure (OR 0.35; 95% CI 0.15-0.86, P = 0.018) among patients with diabetes. Finally, among patients with diabetes, Hp 1-1 was associated with smaller infarct size. This study demonstrates that in patients with diabetes and AMI, the Hp type is an important determinant of clinical outcome and infarct size.

Should primary percutaneous coronary intervention be the preferred method of reperfusion therapy for patients with renal failure and ST-elevation acute myocardial infarction?

Data from patients who had ST-elevation acute myocardial infarction and renal failure and were enrolled in the 2002 Acute Coronary Syndrome Israeli Survey (ACSIS) were studied to determine the effect of different myocardial reperfusion modalities on short- and long-term outcomes. Thirty-day crude mortalities were 8.3% in the thrombolysis group, 40.0% in the primary percutaneous coronary intervention group, and 29.7% in the no-reperfusion group (p = 0.03). Crude and adjusted mortality odds ratios that were observed at 7, 30, and 365 days, with the thrombolysis group as the reference, were 3.1 to 8.1 in the percutaneous coronary intervention group and 1.5 to 4.6 in the no-reperfusion group. Our results suggest that thrombolysis may represent the preferred modality of reperfusion therapy in patients with renal failure and ST-elevation acute myocardial infarction. A large randomized prospective study is needed to confirm these results.

Severe burns in a patient after out-of-hospital CPR.

We present a case of a patient after prolonged cardio-pulmonary resuscitation on hot asphalt, who suffered from first and second degree burns which worsened during hospitalization. The patient was treated with therapeutic hypothermia. Possible effect of therapeutic hypothermia on the course of burns is discussed.

Heart failure in patients with diabetes undergoing primary percutaneous coronary intervention.

INTRODUCTION: Diabetes mellitus is associated with increased risk after acute coronary syndromes. Primary percutaneous coronary intervention is the most effective method of reperfusion for acute ST-elevation myocardial infarction and can limit the ischaemic damage to the left ventricle. However, there are few data on the impact of diabetes mellitus on the risk of heart failure following primary percutaneous coronary intervention. METHODS: We studied 958 ST-elevation myocardial infarction patients treated with primary percutaneous coronary intervention, of whom 263 (27.5%) had diabetes mellitus, with 67 (7.0%) treated with insulin. The primary end points of the study were re-admission for heart failure. Secondary end points were all-cause mortality and recurrent infarctions. The follow-up period was 5 years after hospital discharge. RESULTS: The cumulative incidence of re-admission for heart failure was 8.4%, 15.2% and 26.7% in patients without diabetes mellitus, non-insulin-treated and insulin-treated diabetes mellitus, respectively. Compared with patients without diabetes mellitus, the adjusted hazard ratio for heart failure was 1.95 (95% confidence intervals 1.30-2.93) and 3.09 (95% confidence intervals 1.71-5.60) in non-insulin-treated and insulin-treated diabetes mellitus, respectively. The corresponding hazard ratios for mortality were 1.03 (95% confidence intervals 0.68-1.55) and 2.04 (95% confidence intervals 1.22-3.42), respectively. There was a J-shaped association between fasting glucose levels in the acute phase and risk of mortality (P=0.0001) and a direct association with heart failure (P=0.03). CONCLUSION: Despite modern treatment of ST-elevation myocardial infarction and high levels of guideline-based medical care, diabetes mellitus had an independent adverse effect on the risk of re-admissions for heart failure, which was particularly high among insulin-treated patients.

Time Dependence of the Effect of Right Ventricular Dysfunction on Clinical Outcomes After Myocardial Infarction: Role of Pulmonary Hypertension.

BACKGROUND: The clinical importance of right ventricular (RV) function in acute myocardial infarction is well recognized, but the impact of concomitant pulmonary hypertension (PH) has not been studied. METHODS AND RESULTS: We studied 1044 patients with acute myocardial infarction. Patients were classified into 4 groups according to the presence or absence of RV dysfunction and PH, defined as pulmonary artery systolic pressure >35 mm Hg: normal right ventricle without PH (n=509), normal right ventricle and PH (n=373), RV dysfunction without PH (n=64), and RV dysfunction and PH (n=98). A landmark analysis of early (admission to 30 days) and late (31 days to 8 years) mortality and readmission for heart failure was performed. In the first 30 days, RV dysfunction without PH was associated with a high mortality risk (adjusted hazard ratio 5.56, 95% CI 2.05-15.09, P<0.0001 compared with normal RV and no PH). In contrast, after 30 days, mortality rates among patients with RV dysfunction were increased only when PH was also present. Compared with patients having neither RV dysfunction nor PH, the adjusted hazard ratio for mortality was 1.44 (95% CI 0.68-3.04, P=0.34) in RV dysfunction without PH and 2.52 (95% CI 1.64-3.87, P<0.0001) in RV dysfunction with PH. PH with or without RV dysfunction was associated with increased risk for heart failure. CONCLUSION: In the absence of elevated pulmonary pressures, the risk associated with RV dysfunction after acute myocardial infarction is entirely confined to the first 30 days. Beyond 30 days, PH is the stronger risk factor for long-term mortality and readmission for heart failure.

Inhospital and 1-year mortality of patients who develop worsening renal function following acute ST-elevation myocardial infarction.

BACKGROUND: Recent studies have emphasized the prognostic value of baseline creatinine or estimated creatinine clearance in the setting of acute coronary syndromes. However, the prevalence and prognostic significance of worsening renal function (WRF) in patients with acute ST-elevation myocardial infarction are unknown. METHODS: We studied 1038 patients presenting with acute ST-elevation infarction. WRF was defined as an increase of > or =0.5 mg/dL in creatinine level at any point during hospital stay. The relation between WRF and subsequent inhospital and 1-year mortality was analyzed by use of multivariate logistic regression and Cox proportional hazards models, respectively, controlling for covariates. RESULTS: WRF occurred in 98 (9.6%) patients during hospital stay. Baseline renal dysfunction (calculated glomerular filtration rate <60 mL/min) and WRF were strong independent predictors of inhospital mortality (adjusted odds ratios 2.8, 95% CI 1.3-5.9; and 11.4, 95% CI 6.6-19.5, respectively). In a Cox multivariate analysis, both baseline renal dysfunction (adjusted hazard ratio 2.8, 95% CI 1.6-4.9) and WRF (adjusted hazard ratio 7.2, 95% CI 4.9-10.4) remained independent predictors of 1-year mortality. WRF provided incremental prognostic value toward the prediction of 1-year mortality when added to clinical risk predictors and baseline renal function. The increased mortality associated with impaired baseline renal function was largely caused by events occurring in patients with WRF. CONCLUSION: WRF occurring during admission for ST-elevation myocardial infarction is a powerful and independent predictor of inhospital and 1-year mortality. Small elevations of serum creatinine may serve as a simple marker to identify patients at a very high risk.