EKG Changes Research Articles

Coronary Vasospasm Mimicking ST-Elevation Myocardial Infarction in a Patient With ATRA-Induced Differentiation Syndrome: A case Report and Review of Literature

All-trans retinoic acid (ATRA) has revolutionized the treatment of acute promyelocytic leukemia (APL). Differentiation syndrome is a frequent side effect of ATRA seen in patients with APL. We describe a case of chest pain with inferior ST elevations in a patient with ATRA induced differentiation syndrome. Patient was rushed for cardiac catheterization but his pain and EKG changes resolved after nitroglycerine administration in the catheterization lab. His coronary angiogram did not show any significant lesions raising concern for coronary vasospasm as the underlying cause for pain and EKG changes. Only one case of ATRA related MI has been described in literature before. doi: http://dx.doi.org/10.4021/jh58w

Massive Pulmonary Embolism With ST Elevation in Leads V1-V3 and Successful Aspiration Thrombectomy: Case Report and Review of EKG Changes in Acute Pulmonary Embolism

Massive Pulmonary Embolism With ST Elevation in Leads V1-V3 and Successful Aspiration Thrombectomy: Case Report and Review of EKG Changes in Acute Pulmonary Embolism

Acute regional myocarditis with normal ventricular wall motion diagnosed by two-dimensional speckle tracking imaging

Acute regional myocarditis with normal ventricular wall motion diagnosed by two-dimensional speckle tracking imaging

The Author Response: Suspected Anaphylactic Reaction Associated with Microemulsion Propofol during Anesthesia Induction

To the Editor: We prepared a case report entitled 'Suspected Anaphylactic Reaction Associated with a Microemulsion of Propofol during Anesthesia Induction' (1). However, one reviewer commented that we should have considered midazolam (2), remifentanil (3), rocuronium (4), ephedrine (5), dexamethasone (6), epinephrine (7), poloxamer 188 (8), and polyethylene glycol (9) in addition to a microemulsion of propofol (10). The referenced study (10) concerned propofol not a microemulsion of propofol. In that study, tryptase was normal and the patient had the allergy history to soybean, so they speculated the soybean of the intralipid as the cause of anaphylactic reaction. The mentioned study was about hypersensitivity to midazolam (2). In the study, IgE immunoassay result was in normal. But, after 3 months the inspection, result of intradermal test was positive in the midazolam. It is difficult to diagnose Kounis syndrome, which is a type I hypersensitivity initiated from mast cells with degranulation. The source for a referenced study was wrong, because subject of that study was transdermal fentanyl, not remifentanil (3). Li et al.'s report (7) had no relation with hypersensitivity (hypersensitivity reaction). The contents of the study was that bimatoprost lowered ocular hypertension generated by the topical dexamethasone effectively and the topical dexamethasone raised the ocular pressure falling by the bimatoprost. Of course, all medicines mentioned could directly or indirectly result in a patient's anaphylactic reaction rarely. However, in the present case, since injected drugs prior to the reaction were sequentially remifentanil and microemulsion propofol, the authors illustrated the anaphylactic reaction by microemulsion propofol administration among many factors. The correspondence mentioned that fentanyl could increase IgE mediated anaphylaxis, but because it was not administered to the patient, it seemed not to be an appropriate example. We thought that the cause of the reaction was remifentanil or microemulsion propofol. The skin test was negative and the negative result showed no presence of the IgE antibody. Therefore the non-IgE-mediated anaphylactic reaction was estimated. In addition, PP188 added to a microemulsion propofol has been reported as a cause for a non-IgE-mediated anaphylactic reaction known as the C-activation-related pseudoallergy (11). Of course, the authors do not deny the probability that there could be a false negative reaction. Clinically, we agree that the reaction could be caused by many potential factors not one. The authors did not consider intracoronary mast cell activation (12). In our case, there was no EKG change including ST segment elevation and there was a decrease in blood pressure and tachycardia. We were unable to verify by coronary angiography if there was a vasospasm. The possibility for Kounis syndrome seemed small. The correspondence stated that sulfite was included in the epinephrine, but epinephrine is still the drug of choice for anaphylaxis to sulfite-sensitized patients even though its use is controversial. In addition, we do not have access to preservative-free epinephrine.

The Impact of High Sensitivity C-Reactive Protein Level on Coronary Artery Spasm as Assessed by Intracoronary Acetylcholine Provocation Test

PurposeHigh sensitive C-reactive protein (hs CRP) is well known as a strong risk factor of cardiovascular disease (CVD). The aim of this study is to evaluate the impact of elevated hs CRP on coronary artery spasm (CAS) as assessed by intracoronary acetylcholine (ACh) provocation test.Materials and MethodsA total of 1729 consecutive patients without significant CVD who underwent coronary angiography and intracoronary ACh test between November 2004 and August 2010 were analyzed. The patients were divided into five groups according to quintiles of hs CRP levels.ResultsAt baseline, the prevalence of elderly, hypertension, diabetes mellitus, current smoking, and lipid levels were higher in patients with higher hs CRP. During ACh test, the incidences of significant CAS, ischemic electrocardiography (EKG) change, multivessel, and diffuse CAS were higher in patients with higher hs CRP. Multivariate analysis showed that the old age (OR=1.01, CI; 1.0-1.02, p=0.0226), myocardial bridge (OR=3.34, CI; 2.16-5.17, p<0.001), and highest quintile hs CRP (OR=1.54, CI; 1.12-2.18, p=0.008) were independent predictors of ACh induced CAS. However, there was no difference in clinical outcomes up to 12 months.ConclusionIn conclusion, higher hs CRP was associated with higher incidence of CAS, worse angiographic characteristics and ischemic EKG change, but was not associated with clinical outcomes.

A randomized pilot study of tenofovir/emtricitabine (TDF/FTC) + boosted atazanavir (ATV/r) vs. raltegravir (RAL BID) + ATV/r vs. RAL BID + ATV BID

Patients virologically suppressed on TDF/FTC + ATV/r may require alternative regimens that maintain suppression while addressing some drug‐related side effects. We explored two alternative regimens that replace RTV and/or TDF/FTC. This open‐label exploratory pilot trial enrolled 43 patients on TDF/FTC + ATV/r. Subjects were randomized to one of three arms. Arm 1 (n=15) replaced TDF/FTC with RAL 400 mg BID while continuing ATV/r. Arm 2 (n=14) made two changes: TDF/FTC was stopped and RAL BID was used instead; ritonavir was stopped and ATV 300 mg BID was used. Arm CTL (n=14) continued the baseline (BL) regimen. The week 48 final endpoint is summarized. The primary endpoint was maintaining virologic suppression (&lt;40 c/mL); secondary endpoints compared safety measures. Overall mean age was 46, with 74% Caucasian, 21% black race and 12% female; similar characteristics noted across arms. Through week 48, all but two patients maintained virologic suppression; both virologic failures (&gt;200 c/mL on two consecutive tests) were on arm 2; both reported adherence problems and no resistance mutations were detected. Overall CD4 counts were 534/mm3 at BL and 555/mm3 at week 48. There was a significant CD4 cell count difference favoring CTL (+52/mm3) vs. arm 2 (−14/mm3), p=0.03. No significant differences across arms were noted in lipid fractions or other lab tests. There were no clinically significant EKG changes across arms. Among AEs of interest through week 48, there were more neurologic AEs on arm 1 (n=7) and 2 (n=6) vs. CTL (n=1), and more musculoskeletal events noted on arm 2 (n=7) vs. arm 1 (n=3) and CTL (n=1). Quality of life was measured with a self‐assessment Likert scale. Scores were similar across arms despite the BID dosing in two arms. Self‐reported adherence using 3‐day recall was&gt;95% in all three arms at both baseline and week 48. In this randomized pilot study, two of the three arms maintained virologic suppression in all subjects; there were two virologic rebounds in arm 2. No resistance mutations were detected in either, and adherence issues were noted for both subjects. We also noted that the CD4 cell change was significantly less on arm 2, and there were more neurologic and musculoskeletal AEs on arm 2 vs. CTL. In this study, the use of ATV/r with either TDF/FTC or RAL was successful over 48 weeks, but unboosted BID ATV 300 mg+BID RAL 400 mg as an alternative in virologically suppressed patients should be used with caution.

Apical ballooning in patients with coronary artery disease versus takotsubo cardiomyopathy—A case control study

Takotsubo cardiomyopathy (TC) tends to mimic acute coronary syndrome (ACS) in its clinical presentation. The most common mode of presentation of TC is chest pain or dyspnea precipitated by physical or emotional stress and accompanied by EKG changes (Twave inversion, QT prolongation, transient anteroseptal Q wave, ST segment changes) and elevation of cardiac enzymes [1]. Previous studies have indicated a distinct biochemical marker profile (CK, CKMB, troponins, myoglobin, BNP) in TC and ACS [2–5]; however, data on the differences between TC and LV apical ballooning associated with CAD is sparse. In the present studywemade an attempt to identify unique features differentiating the two conditions. We identified all patients with ‘apical ballooning’ who presented with chest pain. The patients were investigated for ACS, from our echo database (1999–2010—a total of N50,000 records). We then identified those with non-obstructive CAD and other typical findings of takotsubo disease as per the modified Mayo Clinic criteria and defined them as the ‘case’ group (T) (n=11) [6]. From the same database we identified the patients with apical ballooning and obstructive CAD on angiography (N/=50% stenosis of left main coronary or N/=70% stenosis of any coronary with diameter of 2 mm or more). We confirm the arteriographic findings by review of the original images. We selected age, sex and ejection fraction matched controls (C) in a 1:1 ratio (n=11) from that group (baseline features, Table 1); and compared biomarkers as well as echo findings (extracted in duplicate with mean readings included to eliminate interobserver variability) to identify differentiating features between the two groups. All biomarkers were drawn within 24 h of admission and the methods for estimating the levels of various biomarkers did not change during the course of the study. Continuous variables were compared using means; while discrete variables were expressed as ‘percentages’ for comparison using T test. All analyses were performed using Stata Ver 11. The authors of this manuscript have certified that they comply with the Principles of Ethical Publishing in the International Journal of Cardiology. Patients with true takotsubo had significantly higher inflammatory markers (neutrophil count, hsCRP); as well as BNP and myoglobin. However ACS patients had higher troponin levels and acute valvular disease (acute decompensation of valvular function from baseline, i.e., valvular incompetence) was more prevalent (Table 2). Our results show that the higher levels of BNP, inflammatory markers (leukocyte count, neutrophil/lymphocyte ratio, hs-CRP) and serum myoglobin in TC might be able to differentiate TC from LV apical ballooning associated with CAD in a non invasive way. In our study, the levels of BNP and myoglobin were considerably higher in TC as compared to CAD even though the degree of myocardial damage and necrosis was less in TC. Our results are in consensus with previous studies which also show elevated levels of BNP in TC patients [3,5,7]. Regional wall stress secondary to observed basal hyper contractility in TC could be the reason behind the associated high levels of BNP and myoglobin [8]. Another important finding in our study is the higher concentration of inflammatory markers in TC which is in consensus with previous studies [2,9–14]. The difference in pathogenesis of LV apical ballooning associated with CAD and TC could explain our findings, with the latter being predominantly an inflammatory process. The role of inflammation in TC has been established on endomyocardial biopsies and has been supported by elevated levels of various serological and radiological markers (T2 ratio, global relative enhancement) of inflammation; but whether this inflammation is a primary phenomena or secondary to sympathetic overdrive, viral infection or microvascular obstruction, still remains unclear [2,9–15]. Our study has few important limitations. Similar to previous studies, it is a single center study and has a small sample size, so extrapolation of findings to other study populations should be performed with caution. Our control group has a much higher prevalence of functional valvular heart disease (81.8% vs. 9.1%), whichmay act as a confounding factor, thus it may be possible that the actual difference in the level of marker of wall stress like BNP may be even higher between the two groups. Another limitation is that we do not have data on othermarkers of inflammation, especially markers of platelet and monocyte activity and interleukins levels which have been shown to be helpful in differentiating ACS/CAD and TC in previous studies. Our results show that higher inflammatory markers as well as elevated BNP and serum myoglobin can differentiate TC from LV apical ballooning associated with CAD without ICA and may have important clinical implications in subsets of patients who are at higher risk of developing ICA related complications. Further large scale prospective studies are required to establish the role of inflammatory marker, BNP and myoglobin in the diagnostic algorithm of TC in different clinical settings.

Stent Selection in Patients with Myocardial Infarction: Drug Eluting, Biodegradable Polymers or Bare Metal Stents?

Percutaneous coronary intervention (PCI) has been increasingly used in the last years during interventional procedures in patients with acute coronary syndromes (ACS) including ST elevation myocardial infarction (STEMI) and non-ST elevation myocardial infarction (NSTEMI). In patients with either STEMI, NSTEMI, high risk ACS with EKG changes or cardiac enzymes rises; PCI with bare metal stent (BMS) implantation has been associated with a significant improvement in clinical outcome. Therefore, BMS implantation during primary PCI in STEMI has become a standard of practice. With the introduction of drug eluting stents (DESs) in this decade, the use of these new devices instead of BMSs in patients with STEMI has emerged as a rational PCI alternative in this particular subgroup of patients. In spite of the unquestionable benefits of DESs in terms of reduction of restenosis and TVR, specific concerns have arisen with regard to their long-term safety. High incidence of very late stent thrombosis has been described with these devices, and special attention should be paid in patients with unstable coronary lesions, in which plaque composition and remodeling may play a main role in their safety and long-term outcome. Intraluminal thrombus caused by plaque rupture is the most frequent mechanism of STEMI, in which the necrotic core and thin fibrous cap play a major role. In this context, the use of first DESs designs may be futile or even unsafe because delayed healing may further contribute to plaque instability. Adjunctive invasive imaging tools can improve stent deployment and safety outcome in these lesions with intravascular findings of plaque instability. Recently, other players such as new dedicated antithrombotic BMS designs, including selfexpanding stents or drug-eluting coated balloons, are exploring their potential indications in patients with ACS and myocardial infarction. This paper reports and discusses new stent devices and adjunctive pharmacologic agents. It also mentions and describes the recent patents of devices invented to use in these complex lesions subsets.

Myo-Pericarditis and Congestive Heart Failure Secondary to Mesalamine Use Associated With Completely Reversible Cardiac Dysfunction

Mesalamine is a 5-ASA d erivative commonly used to treat ulcerative colitis and mild to moderate crohn’s disease. Rarely, it has been associated with myocarditis or pericarditis. Several hypotheses have been proposed but the exact mechanism of cardiac injury is still unclear. We present a case of combined pericarditis and myocarditis in a young man on mesalamine therapy, with subsequent deterioration of cardiac function, EKG changes and signs of congestive heart failure. After the appropriate treatment, beginning with discontinuation of mesalamine, he had complete recovery of cardiac function to normal. This case exemplifies the importance of quick physician recognition of the disease association and immediate discontinuation of the drug for more successful outcomes in conjunction with appropriate management. doi:10.4021/jmc617w

Regadenoson cardiovascular magnetic resonance myocardial perfusion imaging predicts need for future revascularization

Summary Regadenoson is a new vasodilator myocardial stress agent that is easier-to-use and more tolerable than adenosine. We demonstrate that, in patients undergoing cardiovascular magnetic resonance myocardial perfusion imaging, regadenoson is safe and effective in producing hyperemia and identifying the need for future revascularization. Background Regadenoson (Lexiscan; Astellas) is a new vasodilator myocardial stress agent that selectively activates the A2A receptor. Unlike adenosine, regadenoson is easier to administer and results in fewer side effects. Although extensively studied in patients undergoing nuclear myocardial perfusion imaging (MPI), its performance in cardiovascular magnetic resonance (CMR) MPI remains unknown. The aim of this study was to assess the safety and tolerability of regadenoson and determine its ability to produce hyperemia and predict subsequent coronary revascularization in patients undergoing CMR-MPI. Methods 120 patients were prospectively enrolled to receive CMR-MPI (Achieva, Philips 1.5T) with regadenoson. Patients with contraindications to CMR-MPI or regadenoson were excluded. Short-axis slices were obtained at three levels of the left ventricle (LV) during first pass of Gadolinium-DTPA(0.075 mmol/kg at 4 ml/sec) for 50 consecutive heart beats. Images were acquired using a hybrid gradient echo/echo planar imaging sequence. Imaging was performed 1 minute after injection of regadenoson (0.4mg) and then repeated 15 minutes after injection of aminophylline (125mg) under resting conditions. Perfusion defects were defined as subendocardial hypointensity in a coronary distribution at stress, involving ≥25% wall thickness, and persisting for ≥ 2h eart beats following peak enhancement of the LV cavity. In a subgroup of patients (n=99), custom software was used to generate time intensity curves and to compare the myocardial upslope of the midventricular slice during stress and rest. All subjects were followed for 3 months for the occurrence of coronary revascularization. Results Overall, 51/120 (43%) of patients were female with an average age of 55±15 years and body mass index of 29 ±6 kg/m2. Baseline patient characteristics include: coronary artery disease (33%), diabetes (38%), hypertension (56%), and hypercholesterolemia (95%). The average resting blood pressure and heart rate were 124/ 61mmHg and 70bpm, respectively. Peak heart rate after regadenoson administration was 98bpm (p<0.001). Most patients (87%) experienced side effects from regadenoson including shortness of breath (34%), flushing (23%), and chest discomfort (17%). No EKG changes or residual side effects persisted in any patient at completion of study. The average myocardial upslope increased significantly between rest and stress conditions (9.1±5.9 vs. 12.8±8.1, p<0.001), reflecting the expected hyperemic effect of regadenoson. Perfusion defects were visually apparent in 33/120 (28%) patients. Revascularization occurred in 8/120 (7%) patients (Figure 1). The presence

Electrocardiogram manifestations in hyperkalemia

Hyperkalemia is defined as serum potassium level of more than 5 mmol/L. Prompt identification of hyper-kalemia and appropriate management are critical, since severe hyperkalemia can lead to lethal cardiac dysrhythmias. There is a wide range of electrocardiogram (EKG) changes associated with hyperkalemia. The sequence of EKG changes has been previously described with limited information to correlate the level of potassium to a particular change in the EKG. This study aims to describe a correlation between the level of potassium and EKG changes in the presence or absence of certain diagnoses, to determine which EKG finding in the context of level of hyperkalemia, should be considered life-threatening and prompt emergency intervention. If a relationship between serum levels of potassium and EKG changes is significant, clinicians may be able to better monitor and treat hyperkalemic patients. This paper reviews the literature on hyperkalemia, potassium homeostasis and EKG changes attributed to elevated potassium.

Cocaine And Hyperkalemia Unmasked The Electrocardiogram (EKG) Pattern Of Brugada Syndrome

A very few case reports have indicated that hyperkalemia can induce a Brugada pattern in the electrocardiogram (EKG). On the other hand, very rare case reports have indicated that cocaine has precipitated life-threatening arrhythmias associated with development of Brugada syndrome. We present a 26-year old patient with hyperkalemia secondary to muscle damage and renal insufficiency after a reported large intake of cocaine. The electrocardiogram showed a Brugada pattern. These EKG changes disappeared directly after normalization of serum potassium. We concluded that cocaine and the hyperkalemia were probably the culprit causes of the Brugada-pattern EKG. Unfortunately, the provided data in this case appear to be incomplete; the patient was found unresponsive at home, and we do not exactly whether or not he developed a cardiac arrest secondary to a malignant arrhythmia before the arrival of the Emergency medical services. This case highlights the importance of recognizing cocaine and hyperkalemia as potentialtriggers of the acquired Brugada-like electrocardiographic pattern.

Myo-Pericarditis and Congestive Heart Failure Secondary to Mesalamine Use Associated With Completely Reversible Cardiac Dysfunction

Mesalamine is a 5-ASA derivative commonly used to treat ulcerative colitis and mild to moderate crohn’s disease. Rarely, it has been associated with myocarditis or pericarditis. Several hypotheses have been proposed but the exact mechanism of cardiac injury is still unclear. We present a case of combined pericarditis and myocarditis in a young man on mesalamine therapy, with subsequent deterioration of cardiac function, EKG changes and signs of congestive heart failure. After the appropriate treatment, beginning with discontinuation of mesalamine, he had complete recovery of cardiac function to normal. This case exemplifies the importance of quick physician recognition of the disease association and immediate discontinuation of the drug for more successful outcomes in conjunction with appropriate management. J Med Cases. 2012;3(3):214-216 doi: https://doi.org/10.4021/jmc617w

Treatment and pathogenesis of acute hyperkalemia

This article focuses on the pathogenesis, clinical manifestations, and various treatment modalities for acute hyperkalemia and presents a systematic approach to selecting a treatment strategy. Hyperkalemia, a life-threatening condition caused by extracellular potassium shift or decreased renal potassium excretion, usually presents with non-specific symptoms. Early recognition of moderate to severe hyperkalemia is vital in preventing fatal cardiac arrhythmias and muscle paralysis. Management of hyperkalemia includes the elimination of reversible causes (diet, medications), rapidly acting therapies that shift potassium into cells and block the cardiac membrane effects of hyperkalemia, and measures to facilitate removal of potassium from the body (saline diuresis, oral binding resins, and hemodialysis). Hyperkalemia with potassium level more than 6.5 mEq/L or EKG changes is a medical emergency and should be treated accordingly. Treatment should be started with calcium gluconate to stabilize cardiomyocyte membranes, followed by insulin injection, and b-agonists administration. Hemodialysis remains the most reliable method to remove potassium from the body and should be used in cases refractory to medical treatment. Prompt detection and proper treatment are crucial in preventing lethal outcomes.

Abstract 8734: The Utility of Troponin I in Two Cohorts of Cardiac Patients: Implications for Clinical Practice

Background: Minor elevations in troponin I are common among patients with chronic coronary artery disease (CAD) and those with new supraventricular tachyarrhythmia (SVT). These troponin I elevations are often attributed to an acute coronary syndrome (ACS). However, minor elevations in troponin I may be present for other reasons, such as demand ischemia. Our aim was to observe the prevalence of troponin I elevations in patients with: 1) new onset atrial fibrillation (A-fib), flutter (A-flutter) or SVT and 2) known CAD following exercise, and to assess the hypothesis that troponin I elevations in these settings would not be indicative of ACS. Methods: This study included two components. First, a retrospective review of 740 charts of patients with new onset A-fib, A-flutter or ectopic SVT presenting to the Danbury Hospital Emergency Department between July 2009 and July 2010. Excluded were 45 patients with symptoms and EKG changes indicating ACS on admission. Second, a separate sample of 75 patients with known CAD presenting to the Danbury Hospital Cardiology Clinic for follow-up imaging stress tests were recruited. Eligible patients underwent a stress test and perfusion imaging and had one troponin I sample drawn prior to the stress test and a second at the completion of all imaging four hours later. Results: Among patients with new A-fib, A-flutter and SVT, 31.9% had minor elevations in troponin I levels (values ranged from 0.05-1.0 ng/mL). In those with elevation, 64% had no documented CAD. In addition, for those with elevation, 78.4% had new onset A-fib, 11.3% had new onset A-flutter and 10.4% had new onset SVT. In the separate cohort of patients with CAD who underwent stress testing, 38.7% had troponin elevation following exercise. A total of 50.7% of these patients had no evidence of ischemia by EKG and perfusion and 54.7% had a Duke Treadmill score greater than or equal to 5. Conclusion: For patients with chronic CAD subject to physical stress or those with new onset A-fib, flutter or SVT, small elevations in troponin I are fairly common, and often do not indicate ACS. In a cost containment environment, expensive therapy and testing of these patients may be unnecessary.

Abstract 9218: Troponin Elevation, Ischemic Electrocardiographic Changes and Prognosis after a Postoperative Myocardial Infarction

Background: In the postoperative period the majority of myocardial infarctions are clinically silent and its diagnosis relies heavily on a biomarker elevation. Although an elevated troponin level following vascular surgery is associated with a poor long-term outcome, the utility of abnormal EKG changes as additional prognostic information is unclear. Methods: Single center registry of 435 patients undergoing high-risk vascular surgery at the Minneapolis VA Medical Center between January 2005 and December 2009. Blood was obtained in all patients in the first two days following vascular surgery and the troponin I levels were measured by the Dade Behring Dimension Analyzer. Those values that exceeded the URL were categorized as either LOW (+) (≥ the URL but &lt; 3 times the URL) or HIGH (+) (≥ 3 times the URL). Electrocardiograms obtained before the operation and within the first 3 postoperative days were reviewed by 2 independent cardiologists and classified as ischemic (ST-segment depression, ≥ 2 mm T-wave inversion) or non-ischemic. Long-term survival was retrieved using BIRLS. Results: The mean age of the population was 68±8 and the most common vascular problem was an expanding abdominal aneurysm (49%). Eighty-one (18.6%) patients were classified as HIGH (+) and 104 (24%) as LOW (+) with regard to troponin values. Thirty-one (7%) patients had evidence of myocardial ischemia on electrocardiography. An increase in mortality was seen with incremental troponin values (p &lt;0.001). However, the presence of electrocardiographic changes did not provide additional prognostic information to that conveyed by troponins in any category (p: 0.91, Figure). Conclusions: The requirement for an electrocardiographic correlate of myocardial ischemia to define a myocardial infarction appears to be insensitive in the post-operative period. Further, in the presence of a troponin elevation the incremental prognostic value of an ischemic ECG is minimal.

Abstract P337: Prediction of In-Hospital Major Bleeding Among Patients With Acute Myocardial Infarction: Results From 90,273 Patients in the Acute Coronary Treatment Intervention Outcomes Network Registry®- Get With the Guidelines™ (AR-G)

Background: Bleeding is a common complication of acute myocardial infarction (AMI) management and is associated with worse outcomes. Risk estimation is important to guide choice and intensity of therapy and minimize bleeding-related adverse events. Methods: Using AR-G data, an in-hospital major bleeding model and risk score was developed. Major bleeding was defined as a HCT drop &gt;12%, ICH, retroperitoneal bleeding or transfusion if baseline HCT &gt;28%, and transfusion if baseline HCT &lt;28% with witnessed bleeding. The model used only baseline variables and was developed (n=72,313) and validated (n=17,960) in STEMI and NSTEMI patients (251 US centers from 1/07 to 12/08). C statistic was tested in the derivation and validation cohorts and across key subgroups. Results: Twelve independent factors were identified: heart rate, baseline hemoglobin, female sex, initial creatinine, older age, EKG changes, heart failure or shock on presentation, diabetes, peripheral artery disease, lower weight, systolic blood pressure, and home warfarin use. The model discriminated in the derivation (c=0.73) and validation (c=0.71) cohorts. A score (0-91) was created for the relative odds for major bleeding. Bleeding risk increased tenfold from lowest to highest score: very low risk (3.9%), low risk (7.3%), moderate risk (16.1%), high risk (29%), and very high risk (40%). This trend was consistent across age, sex, and MI type (Figure). Conclusion: The AR-G bleeding model and score estimates bleeding risk across a broad range of STEMI and NSTEMI patients. The model provides clinicians an easy-to-use aid to facilitate treatment decision making and may ultimately promote better patient outcomes.

How should clinicians interpret cardiac troponin values in patients with ESRD?

Division of Nephrology, Department of Medicine, Veterans Affairs North Texas Health CareSystem, Dallas, TexasCardiovascular (CV) mortality is the predominant cause of death in patients with end-stagerenal disease (ESRD). The cause-specific hospitalization rates for CV events and coronaryrevascularization remain high in chronic dialysis patients (1). Chest pain or anginalequivalents are frequently encountered symptoms in the dialysis unit, and early riskstratification for acute coronary syndrome (ACS) is required, as early intervention such asimmediate reperfusion therapy improves outcomes. The American College of Cardiologyand the American Heart Association guidelines incorporated cardiac-specific troponin T(cTnT) and troponin I (cTnI) in the definition of acute myocardial infarction (AMI) anddeemed troponins as the preferred marker for myocardial injury and early risk stratificationof patients who present with suspected ACS (2). The European Society of Cardiologydefines AMI as “detection of rise and or fall of cardiac biomarkers (preferably troponins)with at least one value above the 99th percentile of the upper reference limits (URL),together with evidence of myocardial ischemia with at least one of the following: symptomsof ischemia, EKG changes indicative of new ischemia, development of pathological Qwaves on EKG, or imaging evidence of new loss of viable myocardium or new regional wallmotion abnormality (3).” The diagnostic utility of troponins in patients with ESRD,however, is challenging because the URL were initially derived in subjects without kidneydisease.It is important to understand the unique biochemical and analytical differences in cTnT andcTnI assays to better interpret these diagnostic tests in patients with ESRD. Sufficientdissimilarity between the amino acid sequences of the skeletal and cardiac isoforms of bothTnT and TnI has allowed development of monoclonal antibody-based immunoassays fortheir detection. cTnT and cTnI have different release kinetics after myocardial injury(biphasic vs. monophasic) because of differential compartmentation in the cardiac myocyte,and it was proposed that the kinetics may be altered in dialysis patients (4). Free cTnT is thepredominant form of released TnT as compared to binary/ternary complexes released withcTnI. Some cTnI is also released in oxidized, phosphorylated, or reduced forms. This mayalter the epitope conformation recognized by the monoclonal antibodies in the assays andaccount for low TnI levels in the serum (4). cTnI assays have been developed using differentmonoclonal/polyclonal antibodies directed to various epitopes or isoforms. Anotherchallenge for developing cTnI assays arises from its instability and high susceptibility toproteolysis. Therefore, standardization is lacking in cTnI assays as compared to cTnT (5).

More Than What It First Appears to Be: Gastric Cancer Masquerading as Hyperemesis Gravidarum

A27-year-old gravida 4, para 3, married, Hispanic, non–English-speaking mother presented on our unit at 15 weeks gestation with hyperemesis gravidarum. She was discharged 1 week later on antiemetics and readmitted again 1 week later after fainting. She had electrolyte abnormalities, EKG changes, and severe malnutrition. Despite a droperidol drip she had intractable vomiting. She was noticeably withdrawn and admitted to feeling depressed.

Takotsubo cardiomyopathy vs acute myocardial infarction: diagnostic utility of subtle ECG differences

The clinical findings of Takatsubo Cardiomyopathy and acute myocardial infarction can be very similar. While Takatsubo cardiomyopathy rarely leads to severe complications, acute myocardial infarction can be life threatening. Treatment of both these conditions is different and so it is imperative for clinicians to have a high index of suspicion for either. Several EKG differences between the two entities have been proposed. This article summarizes the EKG changes most likely seen in Takatsubo cardiomyopathy and compares them to those seen in Acute Myocardial infarction.