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A case report of a patient with acute myocardial infarction and severe hypoxemia due to acute right to left interatrial shunt (RLIAS) is presented. Diagnostic and therapeutic procedures are discussed. (Int J Cardiovasc Intervent 2004; 2: 85-87) [ABSTRACT FROM AUTHOR]

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., Competing Interests: Declaration of Competing Interest The authors have no competing interests to declare., (Copyright © 2023 Elsevier Inc. All rights reserved.)

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.

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., (Copyright © 2018 Elsevier B.V. All rights reserved.)

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].

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., (© 2016 S. Karger AG, Basel.)

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., (© 2016 The Authors. Published on behalf of the American Heart Association, Inc., by Wiley Blackwell.)

Right ventricular (RV) infarction is associated with increased mortality. Functional mitral regurgitation (FMR) may complicate inferoposterior infarction with RV involvement leading to pulmonary hypertension and increased RV afterload, potentially exacerbating RV remodeling and dysfunction. We studied 179 patients with inferior wall left ventricular (LV) ST-elevation myocardial infarction and RV infarction. The presence and severity of FMR and RV function were assessed by echocardiography. FMR was diagnosed based on echocardiographic criteria and when the severity of regurgitation was ≥moderate. Eighteen patients (10.0%) had ≥moderate FMR. Estimated pulmonary artery systolic pressure was higher in patients with FMR than in patients without FMR (43 ± 10 vs 34 ± 10 mmHg, respectively, p = 0.002). RV systolic dysfunction was present in 76 patients (42.5%). FMR was a strong predictor of RV dysfunction (odds ratio 5.35, 95% confidence interval [CI] 1.65 to 17.48, p = 0.005) independent of reperfusion therapy. During a median follow-up of 4.1 years, 20 (12.4%) and 10 (55.6%) deaths occurred in patients with and without FMR, respectively (p <0.001). In a multivariable Cox regression model, compared with patients without FMR and with normal RV function, the adjusted hazard ratio for mortality was 1.02 in patients without FMR and with RV dysfunction (95% CI 0.39 to 2.69, p = 0.97) and 3.62 in patients with FMR with RV dysfunction (95% CI 1.33 to 9.85, p = 0.01). In conclusion, in patients with RV infarction, the development of concomitant hemodynamically significant FMR is associated with RV dysfunction. The risk for mortality is increased predominantly in patients with both RV dysfunction and FMR., (Copyright © 2014 Elsevier Inc. All rights reserved.)

Background: Elevated serum phosphorus levels have been linked with cardiovascular disease and mortality with conflicting results, especially in the presence of normal renal function., Methods: We studied the association between serum phosphorus levels and clinical outcomes in 1663 patients with acute myocardial infarction (AMI). Patients were categorized into 4 groups based on serum phosphorus levels (<2.50, 2.51-3.5, 3.51-4.50 and >4.50 mg/dL). Cox proportional-hazards models were used to examine the association between serum phosphorus and clinical outcomes after adjustment for potential confounders., Results: The mean follow up was 45 months. The lowest mortality occurred in patients with serum phosphorus between 2.5-3.5 mg/dL, with a multivariable-adjusted hazard ratio of 1.24 (95% CI 0.85-1.80), 1.35 (95% CI 1.05-1.74), and 1.75 (95% CI 1.27-2.40) in patients with serum phosphorus of <2.50, 3.51-4.50 and >4.50 mg/dL, respectively. Higher phosphorus levels were also associated with increased risk of heart failure, but not the risk of myocardial infarction or stroke. The effect of elevated phosphorus was more pronounced in patients with chronic kidney disease (CKD). The hazard ratio for mortality in patients with serum phosphorus >4.5 mg/dL compared to patients with serum phosphorus 2.50-3.50 mg/dL was 2.34 (95% CI 1.55-3.54) with CKD and 1.53 (95% CI 0.87-2.69) without CKD., Conclusion: We found a graded, independent association between serum phosphorus and all-cause mortality and heart failure in patients after AMI. The risk for mortality appears to increase with serum phosphorus levels within the normal range and is more prominent in the presence of CKD.

Pulmonary hypertension (PH) is usually perceived as a complication of established heart failure (HF) rather than as a predictor of HF or a marker of subclinical HF. PH may develop because of cardiac alterations that result in increased filling pressures after acute myocardial infarction (AMI). We hypothesized that PH might be a useful marker to predict the risk of HF after AMI. We studied 1,054 patients with AMI. Pulmonary artery systolic pressure (PASP) was estimated using echocardiography at the index admission and PH was defined as a PASP >35 mm Hg. The primary end point was readmission for HF at 1 year. PH was present in 471 patients (44.6%) and was strongly associated with age, decreased ejection fraction, advanced diastolic dysfunction, and moderate/severe mitral regurgitation (p <0.0001 for all comparisons). Area under the receiver operating characteristic curve was significantly higher for estimated PASP (0.74 ± 0.02) compared to other echocardiographic parameters (p = 0.02 to 0.0003). After adjustments for clinical and echocardiographic variables in a Cox model, PH was associated with a hazard ratio of 3.10 for HF (95% confidence interval 1.31 to 2.57, p <0.0001). After adding estimated PASP to a model containing clinical and echocardiographic risk factors, net reclassification improvement was 0.21 (95% confidence interval 0.11 to 0.31, p <0.0001). In conclusion, PASP integrates the severity of multiple hemodynamic determinants of increased left atrial pressures that lead to an increase in pulmonary venous pressure. In AMI, PH at the index admission is a useful marker in unmasking latent subclinical HF and predicting the development of overt HF., (Copyright © 2012 Elsevier Inc. All rights reserved.)

Background: Several studies indicated that an elevated body mass index (BMI) is associated with a lower rate of mortality in patients with acute myocardial infarction (AMI). However, the existence of the obesity paradox in AMI patients remains controversial., Methods: We examined the association of BMI and clinical outcomes in 2157 patient with AMI (mean follow-up of 26 months). BMI was categorized into 9 groups (<18.5, 18.5 to 20.9, 21.0 to 23.4, 23.5 to 24.9, 25.0 to 26.4, 26.5 to 27.9, 28.0 to 29.9, 30.0 to 34.9, and ≥35.0 kg/m2). Cox regression was used to calculate hazard ratios (HR) for the various BMI categories, adjusting for the clinical variables, left ventricular ejection fraction, and hemoglobin level., Results: BMI had a U-shaped association with mortality. Relative to the lowest mortality group (BMI of 26.5 to 27.9 kg/m2), the adjusted HRs for mortality were increased only in the lower (HR 2.3; 95% CI 1.3-4.2) and upper (HR 1.8; 95% 1.2-2.9) BMI categories. There was a significant interaction between BMI and anemia (P=0.0003) such that the U-shaped relationship between BMI and mortality was present mainly in patients with anemia. Patients in the lower and upper BMI categories and concomitant anemia had a striking increase in mortality (adjusted HR 5.1, 95% CI 1.9-11.7 and 3.2, 95% CI 1.5-7.0, respectively)., Conclusion: Both obesity and underweight are associated with increased mortality in patients with AMI. The risk of mortality is particularly high among underweight and obese patients with anemia., (Copyright © 2010 Elsevier Ireland Ltd. All rights reserved.)

Aims: Worsening renal function in patients undergoing percutaneous coronary intervention (PCI) for ST-elevation myocardial infarction (STEMI) is associated with adverse clinical outcomes. We hypothesised that platelet glycoprotein IIb/IIIa receptor inhibitors (GPI) may decrease the rate of renal function deterioration in these patients through attenuation of platelet aggregation and the possible improvement of renal rheology and haemodynamics., Methods and Results: Based on prospectively collected data, we analysed rates of renal function deterioration in 603 consecutive patients (mean age 58+/-13 years, males 82%) with STEMI treated with primary or rescue PCI. Renal function deterioration was defined as an increase in serum creatinine level of >or=25% and/or >or=0.5 mg/dl at any time point post-PCI during index hospitalisation compared with baseline value. Outcomes were stratified by treatment with GPI. Patients treated with GPI (n=442) vs. patients who were not treated with GPI (n=161) had significantly lower rates of serum creatinine increase of >or=25% compared with baseline (22.9% vs. 31.9%, P=0.02, respectively), of serum creatinine increase >or=0.5 g/dL (4.1% vs. 8.8%, P=0.02). Treatment with GPI was associated with significantly lower mean maximal increase in serum creatinine level compared with baseline value (0.14+/-0.38 vs. 0.25+/-0.45 mg/dL, P=0.005). Rates of major bleeding did not differ significantly between the two groups (7.3% vs. 5.9%; P=0.42), while 30-day mortality was significantly lower in patients treated with GPI (2.3% vs. 7.5%; P=0.005). By multivariable analysis, treatment with GPI was an independent predictor of freedom from renal function deterioration (odds ratio 0.53; 95% confidence interval 0.33-0.86; P=0.01)., Conclusions: In this analysis, administration of GPI to patients with STEMI treated with primary PCI was associated with lower rates of worsening renal function and lower 30-day mortality.

Recent studies suggest that statin therapy reduces hospitalizations for heart failure (HF). However, few data exist regarding the role of statins in preventing HF after acute myocardial infarction (AMI). In addition, the potential impact of left ventricular (LV) ejection fraction (EF) and coexisting functional mitral regurgitation (MR) on the efficacy of statin therapy was not considered. We prospectively studied 1,563 patients with AMI. The primary endpoint was readmission for the treatment of HF. The effect of statin therapy initiated before hospital discharge was evaluated using a Cox model, adjusting for clinical variables, a propensity score for statin therapy, LVEF, and MR grade. Patients with recurrent infarctions were censored. Statins were prescribed in 1,048 patients (67.1%) before hospital discharge. During a median follow-up of 17 months, admissions for HF were lower in patients receiving statins (6.5% vs 14.8%; unadjusted hazard ratio 0.45, 95% confidence interval 0.32 to 0.63, p <0.0001). In a multivariable Cox model, statin therapy was associated with a significant reduction of hospitalization for HF (HR 0.62, 95% confidence interval 0.43 to 0.89, p = 0.009). There was a significant interaction between MR and statin therapy (p = 0.039), such that the beneficial effect of statins on HF hospitalizations was most pronounced in patients without concomitant MR and absent in patients with hemodynamically significant MR. In conclusion, in patients with AMI statin therapy initiated before hospital discharge significantly reduces subsequent hospitalizations for HF. The effect of statins is driven largely by the reduction in events in patients without concomitant hemodynamically significant MR.

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.

Objectives: This study sought to determine predictors of outcome and examine the influence of baseline risk on therapeutic impact of late mechanical opening of a persistently occluded infarct related artery after myocardial infarction in stable patients., Background: Previous studies in patients with acute coronary syndromes suggest that the impact of infarct-related artery recanalization on clinical outcome is greatest in patients at highest risk., Methods: Of 2,201 patients (age 58.6 +/- 11.0 years) with infarct-related artery occlusion on days 3 to 28 after myocardial infarction in the OAT (Occluded Artery Trial) study, 1,101 were assigned to percutaneous coronary intervention (PCI) and 1,100 to medical therapy alone and followed for a mean of 3.2 years. The primary end point was a composite of death, reinfarction, or New York Heart Association functional class IV heart failure. Interaction of treatment effect with tertiles of predicted survival were examined using the Cox survival model., Results: The 5-year rate for the primary end point was 18.9% versus 16.1% for patients assigned to PCI and medical treatment alone, respectively (hazard ratio [HR]: 1.14, 95% confidence interval [CI]: 0.92 to 1.43, p 0.23). Lack of benefit of PCI was consistent across the risk spectrum for both the primary end point and total mortality, including for the highest tertile (33.9% PCI vs. 27.3% medical treatment alone, HR: 1.27, 99% CI: 0.87 to 1.85 primary end point and 23.5% PCI vs. 21.7% medical treatment alone, HR: 1.16, 99% CI: 0.73 to 1.85 mortality). The independent predictors of the composite outcome were history of heart failure (HR: 2.06, p < 0.001), peripheral vascular disease (HR: 1.93, p 0.001), diabetes (HR: 1.49, p 0.002), rales (HR: 1.88, p < 0.001), decreasing ejection fraction (HR: 1.48 per 10%, p < 0.001), decreasing days from myocardial infarction to randomization (HR: 1.04 per day, p < 0.001), and decreasing glomerular filtration rate (HR: 1.11 per 10 ml/min/1.73 m(2), p < 0.001)., Conclusions: In the OAT study, there was no variation in the effect of PCI on clinical outcomes at different levels of patient risk, including the subset with very high event rates. (Occluded Artery Trial [OAT]; NCT00004562)

Introduction: Renal dysfunction is associated with increased mortality in acute coronary syndromes and other cardiovascular diseases. The prognostic value of kidney dysfunction has been investigated using creatinine-based measures of renal function. Few data are available on the prognostic significance of blood urea nitrogen (BUN), a sensitive marker of hemodynamic alterations and renal perfusion., Methods: The relationship between estimated glomerular filtration rate (eGFR), BUN on admission and changes in BUN during hospital course and long-term mortality was evaluated in 1507 patients with acute ST-elevation myocardial infarction (STEMI)., Results: During a median follow-up of 27 months (range, 12 to 44 months), 281 patients (18.6%) died. In multivariable Cox regression models, elevated BUN (>or=25 mg/dL) at admission was an independent predictor of mortality after adjustments for clinical variables and eGFR (adjusted hazard ratio [HR] 1.7; 95% confidence interval [CI] 1.2-2.3, P=0.0015). Similar results were obtained for elevated BUN/creatinine ratio (>or=25) at admission (adjusted HR 2.0; 95% CI 1.4-2.8; P<0.0001). An increase in BUN 50% above admission value occurred in 260 of patients (17.3%) during hospital course, and was associated with increased risk of mortality after adjustments of clinical variables, eGFR and BUN on admission (HR, 1.7 95% CI 1.3-2.2; P<0.0001)., Discussion: Elevated BUN and BUN/creatinine ratio on admission are independent predictors of long-term mortality in patients with STEMI. An increase in BUN level during hospital course portends adverse outcome independent of eGFR and BUN on admission.

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.

Objectives: We assessed the clinical, electrocardiographic (ECG) and angiographic characteristics of patients with acute coronary syndrome, increased troponin I (cTn-I) levels and normal creatine kinase levels., Background: Cardiac troponins are part of the new definition of acute myocardial infarction by the European Society of Cardiology and the American College of Cardiology. However, there are limited data regarding the angiographic characteristics of these patients., Methods: Between 1/2002 and 7/2004, a total of 50 consecutive cTn-I-positive, creatine kinase-negative patients were admitted to the intensive coronary care unit of our institution and underwent coronary angiography., Results: The mean cTn-I level was 10.7 +/- 13.5 mcg/L and the mean creatine kinase was 106 +/- 40 U/L (normal < 180 U/L). Admission ECG showed inverted T-waves in 42% of patients, ST-segment elevation in 36%, ST-segment depression in 20% and a normal ECG in 20%. A total of 168 lesions were analyzed, and 47 (28%) of these were considered to be nonsignificant lesions (< 50% diameter stenosis). Seven patients had normal or nonsignificant coronary artery disease (CAD) and the remainder had at least single-vessel disease. There were 12 patients with stenosis in the left main coronary artery, 6 patients had a visible clot in the artery, 5 of them located in the right coronary artery and 1 in the left circumflex. A total of 37 patients underwent coronary revascularization, the majority (62%) percutaneously, the rest were treated conservatively., Conclusions: Increased cTn-I levels in the presence of rest pain and normal creatine kinase is not a spurious finding, but may actually be a marker of advanced CAD. However, some of these patients may also have nonsignificant CAD.

Background: Transient hyperglycemia is common during acute myocardial infarction in non-diabetic patients and is associated with a worse outcome. There is limited data on the outcome of patients who undergo primary percutaneous coronary intervention and have transient hyperglycemia., Methods: Fasting plasma glucose was measured in 431 consecutive acute myocardial infarction patients who underwent primary percutaneous coronary interventions. Patients were classified into three groups: non-diabetics/non-hyperglycemic (NDNH, glucose < 126 mg/dL; n=224); non-diabetics/hyperglycemic (NDH, glucose > or = 126 mg/dL; n=119); and diabetics (n=88). Data were analyzed according to the different groups and according to exact glucose levels., Results: In-hospital mortality was significantly lower in NDNH (1%) compared to NDH (8%) and diabetic (5%) patients (p=0.01). One-year cumulative mortality was highest (10%) in patients with NDH (p<0.001). One year target lesion revascularization rates were identical in NDNH and NDH patients (6% vs. 8%) and higher in diabetic patients (19%, p=0.001). In a multivariate model, a striking increase in the risk of death (0.6%, p=0.05) and target lesion revascularization (2%, p<0.0001) was found for every increment of 1 mg/dL in glucose level., Conclusions: Transient hyperglycemia in non-diabetic acute myocardial infarction patients who undergo primary percutaneous coronary interventions is associated with high one-year mortality. One year target lesion revascularization rates were significantly higher in diabetics compared to non-diabetics with normoglycemia or transient hyperglycemia.

Introduction: Elevation of total white blood cells (WBC) count is associated with higher mortality in patients with acute coronary syndromes. However, it is unknown which specific subset of leukocytes best correlates with increased risk of adverse outcome., Methods and Results: We prospectively studied the predictive value of WBC subtypes for long-term outcome in 1037 patients with acute myocardial infarction (AMI). Total WBC, neutrophil, monocyte and lymphocyte counts, and high-sensitivity C-reactive protein (CRP) were obtained in each patient. The median duration of follow up was 23 months (range, 6-42 months). Analyzed separately, baseline total WBC (HR 2.2, 95% CI 1.5-3.3; P<0.0001), neutrophil (HR 2.7, 95% CI 1.8-4.1; P<0.0001) and monocyte (HR 1.9, 95% CI 1.3-2.8; P=0.001) counts in the upper quartile, and lymphocyte count in the lower quartile (HR 1.5, 95% CI 1.1-2.3; P=0.03), were all independent predictors of mortality. Comparing nested models, adding other WBC data failed to improve model based on neutrophil count. In contrast, adding neutrophil count to the models based on total WBC (P=0.01), on monocyte count (P<0.0001) or on lymphocyte count (P<0.0001) improved the prediction of the models. Neutrophil count in the upper quartile (>or=9800 microL(-1)) remained a strong independent predictor of mortality after adjustment for left ventricular systolic function and for CRP (HR 2.2, 95% CI 1.6-3.0; P<0.0001)., Conclusion: Of all WBC subtypes, elevated neutrophil count best correlates with mortality in patients with AMI. Neutrophil count provides additive prognostic information when combined with CRP.

Purpose: To prospectively evaluate the sensitivity of myocardial early perfusion defects (EDs) and late enhancement (LE) at multidetector computed tomography (CT) following acute myocardial infarction (AMI) to predict segment myocardial dysfunction and myocardial functional recovery (MFR), by using echocardiography as the reference standard., Materials and Methods: Institutional review board approval and informed consent were obtained. Twenty-six patients (25 men, one woman; mean age, 53 years+/-9 [standard deviation]), underwent baseline multidetector CT, coronary angiography, and echocardiography within a week of AMI and a follow-up echocardiography at 3 months. ED, LE, and late hypoattenuation were compared with regional left ventricular function and MFR. A logistic regression model and generalized estimating equation analysis were applied to estimate the predictive effect of ED and LE. Differences between groups were evaluated by using nonpaired Student t tests., Results: All EDs and LE corresponded with AMI location determined by using angiography and echocardiography. For occluded arteries (n=5), no relationship was found between the presence of ED or LE and MFR. For patent arteries (n=21), presence of LE had a respective sensitivity and specificity of 73% and 85% for predicting follow-up segment dysfunction, compared with 57% and 90% for ED. In abnormal baseline segments, nonrecovery was clearly related to the presence and size of segment defect area for both ED (odds ratio: 1.95 [95% confidence interval: 0.9, 4.1] per square centimeter) and LE (odds ratio: 1.85 [95% confidence interval: 1.2, 2.9] per square centimeter). Segments that recovered had significantly lower prevalence of ED and LE, and if present, were significantly smaller than in segments remaining abnormal (P<.05)., Conclusion: The presence and size of ED and LE at multidetector CT is closely related to follow-up segment myocardial dysfunction and MFR., (Copyright (c) RSNA, 2007.)

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.

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.

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.

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.

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.

Although percutaneous coronary intervention (PCI) following full-dose thrombolytic therapy (rescue angioplasty) is a common procedure, there is ample controversy regarding the usefulness of the procedure. Moreover, few data are available concerning the safety and efficacy of concomitant treatment with glycoprotein (GP) IIb/IIIa inhibitors in these patients. The aim of the present study was to compare the clinical outcomes of patients who underwent rescue PCI with stents and were treated with GP IIb/IIIa inhibitors. A total of 59 consecutive patients underwent rescue PCI at our institution during the study period, 29 patients (49.2%) were treated concomitantly with a GP IIb/IIIa inhibitor and 30 patients (50.8%) were not. Baseline clinical characteristics were similar between the two groups. In-hospital outcomes regarding death, reinfarction and the need for urgent target vessel revascularization was significantly lower in patients treated with GP IIb/IIIa inhibitors compared to those who were not treated (3.4% vs. 26.7%; p = 0.01, respectively). However, GP IIb/IIIa inhibitor administration was not an independent predictor of better outcomes by multivariate analysis. There was a higher rate of major bleeding complications in patients who received GP IIb/IIIa inhibitors, though it did not achieve statistical significance (6.9% vs. 0%; p = 0.14, respectively). The composite endpoint of major, minor bleeding and vascular complications was similar in both groups (24.1% vs. 16.7%; p = 0.48). In conclusion, the administration of GP IIb/IIIa inhibitors in patients undergoing rescue PCI after failed thrombolysis with stents was safe and may have a beneficial effect on 30-day event-free survival rates, without a significant increase in bleeding or vascular complications. These results warrant further investigation.

We describe two patients with in-stent thrombosis occurring 4 and 21 months after implantation of sirolimus-eluting stents. Both cases occurred following noncardiac surgery. In both cases, aspirin had been stopped prior to surgery. Both patient sustained a severe myocardial infarction; one died. The occurrence of late thrombosis of sirolimus-eluting stents is of concern.

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.

The use of glycoprotein (GP) IIb/IIIa inhibitors during percutaneous coronary interventions (PCI) in the acute phase of myocardial infarction (AMI) is still a matter of debate. The aim of the present study was to compare the outcomes of patients with acute ST-segment elevation myocardial infarction who underwent primary PCI and were concomitantly treated with GP IIb/IIIa inhibitors with those who were not treated with these drugs. Between January 1996 and November 2003, a total of 418 consecutive patients underwent PCI in the setting of ST-segment elevation AMI. At the operator's discretion, 287 patients were concomitantly treated with GP IIb/IIIa inhibitors and 115 patients were not. Angiographic success and final TIMI 3 flow in the infarct-related artery was achieved more frequently in patients treated with GP IIb/IIIa inhibitors (90% vs. 77%; p=0.001). The in-hospital composite endpoint of death, reinfarction and bleeding complications was significantly better in patients treated with GP IIb/IIIa inhibitors (4% vs. 12%; p=0.005). Furthermore, the adjusted 12-month survival rate was significantly better in these patients (RR: 2.99, CI: 1.29-6.9; p=0.01). Therefore, adjunctive therapy with GP IIbIIIa inhibitors during primary PCI is associated with improved short-term outcomes and one-year survival without an increased risk of bleeding.

Purpose: To determine the prevalence and prognostic implications of hyponatremia in the setting of acute ST-elevation myocardial infarction., Methods: The study sample consisted of 1047 consecutive patients presenting with acute ST-elevation myocardial infarction. Plasma sodium concentrations were obtained on admission and at 24, 48, and 72 hours thereafter. Infarct size was determined by echocardiographic examination that was performed on day 2 or 3 of hospitalization., Results: Hyponatremia, defined as a plasma sodium level <135 mmol/L (<135 mEq/L), was present on admission in 131 patients (12.5%) and developed during the first 72 hours of hospitalization in 208 patients (19.9%). Plasma sodium levels decreased to < or = 130 mmol/L in 45 patients (4.3%). In a multivariate logistic regression analysis, hyponatremia was independently associated with 30-day mortality. The risk of 30-day mortality associated with hyponatremia on admission (odds ratio [OR] = 2.0; 95% confidence interval [CI]: 1.0 to 3.9; P = 0.04) was similar to that of hyponatremia developing after admission (OR = 2.4; 95% CI: 1.5 to 4.2; P = 0.002). The risk of 30-day mortality increased with the severity of hyponatremia, with an odds ratio of 2.1 in patients with sodium levels between 130 and 134 mmol/L (95% CI: 1.2 to 3.5; P = 0.007) and 3.4 in those with levels <130 mmol/L (95% CI: 1.5 to 7.8; P = 0.002)., Conclusion: Hyponatremia on admission or early development of hyponatremia in patients with acute ST-elevation myocardial infarction is an independent predictor of 30-day mortality, and prognosis worsens with the severity of hyponatremia. Further studies are required to determine if plasma sodium levels may serve as a simple marker to identify patients at high risk.

Background: The long-term prognosis of diabetic patients with multivessel coronary artery disease (CAD) treated by surgical or percutaneous coronary revascularization is significantly worse as compared to non-diabetics. Lower rates of complete revascularization may be one factor that influences the poor long-term outcome in the diabetic population. Our study assessed the impact of complete revascularization on the long-term prognosis in diabetic patients with CAD treated by percutaneous coronary intervention (PCI). The study included 658 consecutive diabetic patients (mean age, 60.9+/-10.1 years) who underwent PCI. Multivessel disease was present in 352 patients (53.5%). Revascularization was complete in 94 (26.7%) and incomplete in 258 (73.3%) patients with multivessel disease. Reasons for incomplete revascularization included angioplasty of only the culprit lesion (43.4%); small vessel size (22.8%); moderate lesion, defined as diameter stenosis 50-69% (18.6%); chronic total occlusion of the non-intervened vessel (6.6%); and others (8.5%). Overall survival rate at 5 years was 87.4%. Patients who underwent complete revascularization had a 94.5% survival rate, compared to 83.0% for those with incomplete revascularization (p<0.001). Similarly, the rates of myocardial infarction-free survival were significantly higher in patients with complete versus incomplete revascularization (92.9% versus 79.9%, respectively). Incomplete revascularization was the most powerful independent predictor of mortality at follow-up (relative risk 95% confidence interval, 1.54-7.69; p=0.003). Our data suggest that complete myocardial revascularization may improve the long-term prognosis after PCI of diabetic patients with multivessel CAD.

Late stent thrombosis in the era of routine high-pressure stent deployment and combined antiplatelet therapy with thienopyridines and aspirin has become a rare but feared complication. We describe a patient with acute myocardial infarction due to late stent thrombosis 6 weeks after deployment of a sirolimus-eluting stent and 2 weeks after the discontinuation of clopidogrel. This is the first report of late thrombosis of a sirolimus-eluting stent., (Copyright 2003 Wiley-Liss, Inc.)

Stents have revolutionized percutaneous coronary interventions (PCI), impacting on both acute and long-term results. However, despite improvements in stent design, stent deployment failure is not an unusual event. The aim of the present study was to assess the frequency and causes of stent deployment failure, as well as the outcome of these patients. Between 1997 and 2001, a total of 3,537 patients underwent stent-assisted PCI and delivery of 5,275 stents was attempted. In the majority of patients (118; 78.1%), stenting was performed as provisional; in the remaining 33 (21.8%) as a bailout procedure. A total of 175 (3.3%) stents in 151 (4.3%) patients failed. Failure to deliver the stent to the lesion site was the main cause in 139 patients (92%) and failure either to expand adequately the stent or premature disengagement of the stent from the balloon in only 12 patients (8%). Peripheral stent embolization occurred in 10 (0.3%) patients. Deployment of a different stent in place of the failed one was attempted in 122 patients and was successful in the majority (108; 88.5%). In-hospital major adverse cardiac events were observed in six patients (4%): three patients required emergency coronary artery bypass surgery, two had a myocardial infarction (MI), and one patient underwent urgent repeat coronary intervention. At a mean follow-up of 32.2 +/- 17.7 months, 22 major adverse cardiac event occurred in 17 patients (11.2%): 1 cardiac death, 3 patients had an MI, and 18 patients required target vessel revascularization. One-year event-free survival for the whole group was 91.2%. Patients with stent embolization did not have any major adverse cardiac or vascular events. Thus, the rate of stent deployment failure in our series was 3.3%, mainly due to failure to deliver the stent to the site. Another stent was successfully deployed in the majority of cases and these patients had favorable short- and long-term outcomes., (Copyright 2003 Wiley-Liss, Inc.)

Background: Coronary stenting was recently introduced as a primary intervention for acute myocardial infarction. Several randomized controlled studies have shown that stenting may be superior to balloon angioplasty for the treatment of AMI. However, routine stenting may also cause deterioration of coronary flow., Objective: To analyze the clinical characteristics and the outcome of patients who were treated with stenting for AMI in our center in the recent era of stenting., Methods: Fifty-five patients with AMI were treated by stent implantation between January 1998 and December 1999. Adverse clinical events were recorded, including death, recurrent infarction, coronary artery bypass grafting, cerebrovascular accident, and target vessel revascularization. In-hospital, 1 month, 6 month and 1 year follow-up was performed in all patients. Repeat coronary angiography was performed according to clinical indications., Results: Baseline angiographic results showed Thrombolysis in Myocardial Infarction (TIMI) 0 flow in 39 patients (70.9%), TIMI I flow in no patient and TIMI II/III flow in 16 patients (29.1%). TIMI grade 3 flow was achieved in 90.9% of patients at the end of the procedure. In-hospital mortality rate was 5.4% (2.1% in patients without cardiogenic shock). There was no evidence of re-infarction or TVR. The rates of bleeding complication (all of them minor), CVA, and CABG were 9.1%, 3.6% and 1.8% respectively. The 6 month mortality rate remained the same. Rates of re-infarction, restenosis, TVR and CABG were 3.6%, 14.5%, 14.5% and 5.4% respectively. The 1 year mortality rate was 7.3%. Restenosis rate was 18% and CABG 7.3%. One year event-free survival was 70.9%., Conclusions: This study suggests that stenting is a safe and effective mode of therapy in the setting of AMI associated with a high rate of revascularization and a low short and long-term outcome.

Background: Iatrogenic illness, defined as a disease that results from a diagnostic procedure or from any form of therapy, is a well-recognized phenomenon in clinical practice., Objectives: To study and evaluate major cardiac iatrogenic disease as the cause of admission to the intensive cardiac care unit in the modern era., Methods: We assessed 64 critically ill patients suffering from major cardiac iatrogenic problems among a total of 2,559 patients admitted to the intensive cardiac care unit during 3 years. Iatrogenic illness was defined as any problem that resulted from therapy. Only cardiac problems were included in the study. Complications of interventional cardiovascular procedures, suicide attempts or accidental intoxications were excluded., Results: There was evidence of a major cardiac iatrogenic problem as the cause for admission in 64 patients (2.5%): 58 (91%) suffered from arrhythmias (mainly bradyarrhythmias) secondary to beta-blockers, amiodarone, calcium antagonists, electrolyte imbalance or a combination, and 6 (9%) had non-arrhythmic events (hypotension, syncope or acute heart failure). In 41 patients (64%) the iatrogenic event was considered preventable., Conclusions: Major cardiac iatrogenic complications are an important factor among patients admitted to the intensive cardiac care unit. Most of the events are bradyarrhythmias related to anti-arrhythmic agents. Almost two-thirds of events are preventable.

We describe a 66-year-old patient with hemoptysis, a drop in hematocrit, hypoxemia and new bilateral alveolar infiltrates after receiving streptokinase for acute myocardial infarction. Markedly increased carbon monoxide diffusion capacity suggested a diagnosis of alveolar hemorrhage. Underlying conditions included congestive heart failure. The patient recovered uneventfully within 7 days of conservative treatment. Alveolar hemorrhage is a rare and often unrecognized life-threatening complication of thrombolytic therapy. Particular attention should be paid to the pulmonary status of patients with congestive heart failure scheduled to receive thrombolytic therapy., (Copyright 2000 S. Karger AG, Basel)