Evidence Of Wall Motion Abnormalities Research Articles

196 Cardiovascular magnetic resonance characterization of myocardial injury in recovered COVID-19 patients with elevated troponins during hospital stay

AimsDespite being a common finding in hospitalized COVID-19 patients, cardiac troponin elevation remains a nonspecific detection of myocardial injury and further in-hospital investigation into the cause of myocardial injury is rarely done. COVID-19 patients with myocardial injury show a significantly higher in-hospital mortality rate compared with those without myocardial injury and among those with myocardial injury, greater degrees of troponin elevation are associated with higher mortality rates. There are still many questions regarding possible cardiovascular sequelae and prognostic significance in these patients. Being able to distinguish between inflammatory and ischaemic causes of myocardial injury cardiovascular magnetic resonance (CMR) is the non-invasive modality of choice to investigate myocardial involvement in these patients. Presented are the preliminary single-centre results from a multicentre study aimed to characterize the prevalence, type and extent of COVID-19-related cardiovascular sequelae using CMR imaging.Methods and resultsIn this single-centre prospective observational cohort study, patients hospitalized with confirmed COVID-19 and at least one value of high sensitivity I troponin (hs-Tnl) >99th percentile during hospitalization were eligible for follow-up contrast-enhanced CMR imaging. Patients with any standard CMR contraindications were excluded. Images were acquired using a standardized myocarditis protocol including late gadolinium enhancement (LGE) and T1 and T2 mapping. Cutoff values of 1015 ms and 50 ms were used for abnormal T1 and T2 measurements, respectively. Of the 21 patients (65 ± 11.85 years) who underwent imaging, 15 (71.4%) were male. The mean follow-up duration from the date of confirmed COVID-19 diagnosis was 169 ± 19 days. The mean left ventricular ejection fraction was 64.1 ± 13.87 and 3 (14.3%) patients had evidence of wall motion abnormalities. LGE was seen in 9/20 (45.0%) patients, reflecting myocardial fibrosis. Increased native T1 signal representing myocardial fibrosis and/or oedema was seen in 9/20 (45.0%) patients. While increased native T2 signal, being more specific for oedema was observed in 3/20 (15.0%) patients. Considering CMR findings, 6 (28.6%) patients showed evidence of previous myocarditis.ConclusionsIn this single centre Italian study of patients hospitalized with COVID-19 and elevated cardiac enzymes, myocarditis-like injury was evident in about a quarter of the patients. Whether these findings will lead to long-term cardiac complications is still to be confirmed.

CETUXIMAB: A POTENTIALLY UNDER RECOGNIZED ETIOLOGY OF SUDDEN CARDIAC DEATH

TOPIC: Critical Care TYPE: Medical Student/Resident Case Reports INTRODUCTION: Certain medications have been linked to an increased risk of sudden cardiac death through varying mechanisms. Herein, we describe a case of a cardiac arrest where cetuximab was presumed the culprit. CASE PRESENTATION: A 58-year-old female with a history relevant for TxN3bM0 squamous cell carcinoma of the neck on chemoradiation therapy was transferred to the hospital after having a cardiac arrest while receiving cetuximab. She presented earlier to the cancer center with no complaints. During cetuximab infusion, she had a cardiac arrest (pulseless electrical activity). She was resuscitated per ACLS guidelines and had a return of spontaneous circulation (ROSC) within eight minutes. Post ROSC, she was hemodynamically stable, with appropriate oxygenation and ventilation. An electrocardiogram showed normal sinus rhythm with no signs of ischemia. Point of care ultrasonography (POCUS) showed a normal left ventricular ejection fraction, with no evidence of wall motion abnormalities, right ventricular strain, or pericardial effusion. POCUS also ruled out deep vein thrombosis and pneumothorax. Cardiac enzymes, brain natriuretic peptide, potassium, calcium, and magnesium, were normal. Post-cardiac arrest care was provided, including targeted temperature management. The next day, she was following commands and meeting extubation criteria. She was extubated and transferred to the floor one day after. Formal echocardiography confirmed POCUS findings. In the absence of another explanation for her cardiac arrest, cetuximab was to blame. DISCUSSION: Cetuximab is a monoclonal antibody that binds the epidermal growth factor receptor (EGFR), competitively inhibiting the binding of EGF and resulting in inhibition of cell growth and induction of apoptosis. Cetuximab is indicated for locoregionally advanced squamous cell carcinoma of the head and neck (SCCHN) in combination with radiation therapy. The addition of cetuximab in this population increased median overall survival by 20 months1. In patients with SCCHN treated with cetuximab and radiation therapy, 2% had sudden death1. Cardiac arrest also occurred in 3% of SCCHN patients treated with cetuximab in combination with platinum-based therapy and fluorouracil2. As a result, cetuximab's package has "sudden death" as a black box warning. Of note, 50% of patients treated with cetuximab may develop hypomagnesemia, and weekly monitoring of electrolytes is recommended. In our patient, electrolytes were normal, and the exact mechanism of cetuximab-induced cardiac arrest remains unclear. CONCLUSIONS: Cetuximab-induced cardiac arrest occurs in 2%-3% of treated patients in controlled studies. Real-world incidence may be higher. We report this case to add to the literature what we believe is a case of cetuximab-related cardiac arrest. REFERENCE #1: 1. Bonner JA, et. al. New England Journal of Medicine. 2006 Feb 9;354(6):567-78. REFERENCE #2: 2. Vermorken JB, et al. New England Journal of Medicine. 2008 Sep 11;359(11):1116-27. DISCLOSURES: No relevant relationships by Tony Abdo, source=Web Response No relevant relationships by Ammaar Azeem, source=Web Response No relevant relationships by SYED HUSSAIN, source=Web Response

5964Hybrid PET/MR imaging for the prediction of left ventricular (LV) recovery after revascularisation of chronic total occluded coronaries

Abstract Background Percutaneous coronary intervention (PCI) of chronic total occlusion (CTO) represents one of the major challenges in interventional cardiology. Physicians are still reluctant in referring for PCI, assuming non viability of the myocardium subtended by the CTO. Data are controversial in assessing the improvement of left ventricular (LV) wall motion after revascularisation and the prognostic value of viability testing to guide patient selection. Purpose The aim of this study was to determine, whether hybrid fluorodeoxyglucose positron emission tomography/magnetic resonance (FDG PET/MR) imaging allows a more accurate prediction of LV regional wall motion recovery after successful PCI of CTOs in comparison to PET or MR alone. Methods We enrolled 49 consecutive symptomatic patients with CTO and evidence of wall motion abnormality in the corresponding CTO-territory. All patients underwent hybrid FDG PET/MR imaging as semi-quantitative assessment of myocardial viability - glucose metabolism in PET and late gadolinium enhancement (LGE) transmurality in MR – prior of PCI of the CTO. Follow-up MRI was performed in 23 patients 3–6 months after successful revascularisation to evaluate wall motion changes. Results We assessed viability in 124 myocardial segments subtended by a CTO in 23 patients with successful PCI who underwent serial imaging. Segments with wall motion abnormality at baseline (n=80) were analysed. Most of these segments (n=54, 68%) were concordantly assessed viable by PET and MR, conversely only 2 (2%) segments were assessed non-viable by both imaging techniques. However, almost one third of the segments showed discordant patterns of viability either PET not viable/ MR viable (3 (4%) segments) or PET viable/ MR not viable (21 (26%) segments): particularly the latter revealed a significant wall motion improvement (p=0.033). The combination of PET and MR showed a fair accuracy in predicting myocardial segments with wall motion improvement after CTO revascularisation (PET/MR area under ROC curve (AUC) 0.72, SE 0.07, p=0.002), which was superior to MR-LGE (AUC=0.66, SE 0.09) and FDG-PET (AUC=0.58, SE 0.10) alone (Figure). Comparisons of ROC curves Conclusion Hybrid PET/MR imaging prior to successful CTO showed a better performance than PET or MR alone in predicting regional improvement of disturbed wall motion. The complimentary information derived from both modalities may particularly help to identify small amounts of viable epicardial myocardium within large scars which can improve contractility after CTO-revascularisation.

The significance of electrocardiographic changes without echocardiographic evidence of segmental wall motion abnormalities in patients undergoing dobutamine stress echocardiography

Ischemic ECG changes during dobutamine stress echocardiography (DSE) have been reported to have low sensitivity and specificity for detecting myocardial ischemia in the absence of wall motion abnormalities on echocardiography. We present a case of a renal transplant candidate with severe multivessel disease who had ST depressions without any wall motion abnormalities on DSE. Certain studies have shown the sensitivity of DSE is lower in patients with left ventricular hypertrophy and/or end stage renal disease, but the significance of ischemic ECG changes with no evidence of wall motion abnormalities in these patients has not been well studied.

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Ischemic ECG changes during dobutamine stress echocardiography (DSE) have been reported to have low sensitivity and specificity for detecting myocardial ischemia in the absence of wall motion abnormalities on echocardiography. We present a case of a renal transplant candidate with severe multivessel disease who had ST depressions without any wall motion abnormalities on DSE. Certain studies have shown the sensitivity of DSE is lower in patients with left ventricular hypertrophy and/or end stage renal disease, but the significance of ischemic ECG changes with no evidence of wall motion abnormalities in these patients has not been well studied.

Abstract WP263: Wall Motion Abnormalities on Transthoracic Echocardiography in the Setting of Ischemic Stroke Reflect Underlying Cardiac Disease and May Warrant an Ischemic Cardiac Evaluation

Background and Purpose: Patients with acute ischemic stroke (AIS) are at a heightened risk of cardiovascular events. We hypothesize that wall motion abnormalities (WMA) on transthoracic echocardiography (TTE) in the setting of AIS reflect underlying heart disease rather than reversible cardiac strain caused by the stroke. Methods: Data was abstracted from a single center prospective AIS database over 18 months and included all patients with acute ischemic stroke who underwent a TTE. The presence of WMA was abstracted from the TTE report. Univariate analyses and predefined multivariable models were performed to determine factors associated with WMA, including demographic factors (age and sex), risk factors (hypertension, diabetes, hyperlipidemia, history of stroke, atrial fibrillation, congestive heart failure, coronary heart disease, and smoking), NIHSS score, cardiac markers (positive troponin, ECG evidence of prior myocardial infarction, ejection fraction), and insular location of infarct. Results: We identified 1044 patients who met the inclusion criteria; 139 (13.3%) had evidence of WMA, of which only 23 patients had no history of heart disease or ECG evidence of prior myocardial infarction. Among these 23 patients, 12 had a follow up TTE after the stroke and WMA persisted in 92.7% (11/12) of patients. On fully adjusted models, factors associated with WMA are older age (OR per SD 1.03, 95% CI 1.001-1.05; p=0.009), congestive heart failure (OR 4.44, 95% CI 2.39-8.33, p<0.001), history of coronary artery disease or ECG evidence prior myocardial infarction (OR 27.03, 95% CI 14.93-50.0, p<0.001), and elevated serum troponin levels (OR 2.00, 95% CI 1.06-3.75, p=0.031). Conclusion: In AIS patients, WMA on TTE may reflect underlying cardiac disease and warrant further cardiovascular evaluation particularly in those without known history of cardiac disease. Future studies are needed to investigate the cost-effectiveness of this approach.

Pericarditis as a Complication of Acute Colitis: A Case Report

SESSION TITLE: Miscellaneous Global Case Reports SESSION TYPE: Global Case Report Poster PRESENTED ON: Tuesday, October 27, 2015 at 01:30 PM - 02:30 PM INTRODUCTION: Pericarditis has been reported as an extra intestinal manifestation of some inflammatory bowel disease (IBD) including ulcerative colitis, Crohn's disease, intestinal tuberculosis, as well as in nonspecific IBD. Those cases are underreported. We, therefore, describe a case report of pericarditis in conjunction with nonspecific IBD. CASE PRESENTATION: A 46-year-old previously healthy Brazilian woman complained of sudden onset of watery, purulent but non-bloody diarrhea associated with crampy abdominal pain, along with blunt chest pain. EKG showed diffused repolarization alteration and normal troponin t levels. Both echocardiogram (ECO) and cardiac resonance (CR) showed small pericardium effusion. ECO showed 63% ejection fraction and no evidence of wall motion abnormalities. Cardiac catheterization revealed normal coronary arteries. Colonoscopy showed macroscopically congested and eroded mucosa from the terminal ileum to the descending colon, with petechiae indicative of colitis. Microscopic examination of obtained biopsies revealed acute mucosal inflammation with superficial ulceration, without both granulomas and ischemia. Both ASCA and p-ANCA neutrophils exams were normal. The patient was treated with indomethacin 50mg bid, and supportive care. Chest pain improved gradually, and the patient was discharged asymptomatic five days after admission. DISCUSSION: Cardiac complications of inflammatory bowel disease are rare; yet cases of pericarditis, myocarditis, and myopericarditis have been reported. Pericarditis is the most commonly reported complication. In general, viral and idiopathic cases of pericarditis have good prognosis. In our patient, the diagnosis of pericarditis was established on the bases of clinical features, electrocardiographic changes, ECO and CR alterations in the absence of coronary artery abnormalities by cardiac catheterization. CONCLUSIONS: Pericarditis may be a challenging diagnosis, especially when considered as an extra intestinal manifestation of both specific and nonspecific colitis. Reference #1: Myopericarditis as a complication of nonspecific colitis. Alkhateeb H, Said S, Cooper CJ, Elhanafi S, Teleb M, Saifuddin F, Mukherjee D, Abbas A, Davis HE 2nd. Am J Case Rep. 2014 Feb 21;15:82-4. doi: 10.12659/AJCR.890006. eCollection 2014. Reference #2: Pericarditis in exacerbation of ulcerative colitis. Virovic Jukic L, Duvnjak M, Barsic N, Lerotic I, Tomasic V, Pavic T. Acta Gastroenterol Belg. 2006 Oct-Dec;69(4):390-2. Reference #3: Acute pericarditis and ulcerative colitis. Rodríguez Blanco VM, Barriales Alvarez V, Cortina Llosa A. An Med Interna. 1997 Nov;14(11):598-9. DISCLOSURE: The following authors have nothing to disclose: Gilberto Franco, Carlos Alves, Pamela Bianchet No Product/Research Disclosure Information

Acute cardiogenic shock induced by infusional 5-Fluorouracil.

A 49-year-old patient with metastatic carcinoma of the bladder and no prior history of heart disease presented with diffuse ST elevation, elevated troponins, and biventricular dysfunction requiring intensive care unit admission and inotropic support after receiving her first course of infusional 5-fluorouracil (5-FU). Over the course of several days, the patient's cardiac function and clinical status returned to baseline. A follow-up echocardiogram performed 5 days after initial presentation revealed an ejection fraction of 59 percent, with no evidence of wall motion abnormalities. Subsequent 5-FU chemotherapy was discontinued, and the patient went on to receive second-line chemotherapy.

Myopericarditis as a complication of nonspecific colitis

Patient: Male, 31Final Diagnosis: MyopericarditisSymptoms: Abdominal pain • diarrheaMedication: —Clinical Procedure: —Specialty: CardiologyObjective:Unusual setting of medical careBackground:Myopericarditis is a condition involving inflammation of the pericardium and myocardium. It has been reported in conjunction with inflammatory bowel disease as well as infectious colitis caused by a cardiotropic organism. The etiology of myopericarditis includes a long list of infectious causes (especially viral), toxic causes, autoimmune disorders, and vasculitides.Case Report:A 31-year-old previously healthy Hispanic man complained of sudden onset of watery, non-bloody diarrhea associated with mucus and crampy abdominal pain. ECG showed ST-segment elevation in the infero-lateral leads, with elevated troponin I level. Urgent cardiac catheterization revealed normal coronary arteries and the patient was diagnosed with myopericarditis. The echocardiogram results were within normal limits, with 65% ejection fraction and no evidence of wall motion abnormalities. Colonoscopy showed macroscopically congested mucosa in the descending colon, sigmoid colon, and rectum, with scattered petechiae indicative of nonspecific colitis. Microscopic examination of obtained biopsies revealed evidence of acute mucosal inflammation without ulceration, granulomas or ischemia. The patient was started on Naproxen 250 mg twice daily and chest pain started to improve gradually. The patient was discharged on Naproxen and was followed up in clinic 2 weeks after discharge, where he was found to be completely asymptomatic, with troponin level <0.015 ng/ml.Conclusions:Myopericarditis is a challenging diagnosis that has been reported in association with colitis, either as an extraintestinal manifestation of IBD or due to infectious colitis with a cardiotropic organism.

Atypical cause of a typical chest pain.

A 56 year old African American female who had a past medical history of transient ischemic attack in 2006 presented in our emergency department with first episode of sudden onset of severe central chest pain radiating to both arms , exaggerated by exertion, without any relieving factors, associated with nausea and sweating. She was taking baby aspirin, folic acid and multivitamin regularly. She did not have any history of smoking, alcohol or drug abuse. On Examination, she was in moderate distress due to pain, her pulse rate was 110 per minute (regular), and blood pressure was 153/85 mm HG. She was having mild tenderness in left upper quadrant. Rest of the physical examination was benign. Her initial electrocardiogram (EKG) did not show any acute ST segment or T wave changes. Troponin-I was also negative. She was started on oxygen, intra venous morphine and normal saline and shifted to the medical floor for further management. Her serial EKG’s and troponin’s remain negative. Transthoracic echocardiogram did not show any evidence of wall motion abnormalities. Further laboratory data showed that she was having hemolytic anemia with hemoglobin of 9.7 gm/dl and reticulocyte count of 4.8%. Upon further digging into the history, she mentioned that she had been periodically visiting hematology clinic, although she did not remember the reason for that. Once we contacted the

Silent myocardial damage in cocaine addicts

BackgroundCocaine addiction is associated with either ischaemic or non-ischaemic cardiac complications. The prevalence of myocardial damage in asymptomatic addicts has never been evaluated by cardiovascular magnetic resonance (CMR), which allows...

Intermittent changing axis deviation during acute myocarditis

It has been rarely reported intermittent changing axis deviation also during atrial fibrillation and also during atrial flutter. Intermittent changing axis deviation during acute myocardial infarction and changing axis deviation associated with atrial fibrillation and acute myocardial infarction too have been also rarely reported. Conduction system disturbances have been described during acute myocarditis and it has been suggested that myocardial interstitial edema is implicated in the conduction disturbances that occur in acute myocarditis. Usually, edema is located in the epicardial layer of ventricular wall during acute phase of focal myocarditis and it can't be associated with clear evidence of wall motion abnormalities. It has also been described in a work the report of sequences of alternatively normal and Wenckebach beats with alternate and progressive right bundle branch block interpreted as functional longitudinal dissociation in atrioventricular conduction axis during chronic chagasic myocarditis. We present a case of changing axis deviation during acute myocarditis in a 15-year-old Italian man. This case focuses attention on changing axis deviation during acute phase of focal myocarditis in absence of wall motion abnormalities.

Strain Doppler echocardiography can identify longitudinal myocardial dysfunction derived from edema in acute myocarditis

Usually, during acute phase of focal myocarditis, edema is located in the epicardial layer of the ventricular wall and it can't be associated with clear evidence of wall motion abnormalities on echocardiography. Among many cardiac imaging techniques, only cardiac magnetic resonance (CMR) and computer tomography permit a direct detection of edema during acute myocarditis. We report a case where strain Doppler echocardiography was able to identify longitudinal segmental myocardial dysfunction derived from edema in acute phase of myocarditis. The strain Doppler echocardiography was compared with cardiac magnetic resonance.

A Case Report of Absent Right Superior Vena Cava with Persistent Left Superior Vena Cava: Echocardiographic Findings

We hereby report a case of absent right superior vena cava (SVC) with persistent left SVC (PLSVC); the echocardiography findings using contrast (injection of agitated normal saline) are presented. CASE REPORT A 50-year-old woman underwent 2-dimensional echocardiography as part of evaluation of atypical chest pain of a few days’ duration. She did not have any significant medical or surgical history; she had no family history of heart disease. Results from a 12-lead electrocardiogram were within normal limits. The patient was found to have a large dilated coronary sinus measuring 3.2 cm in diameter (Figures 1 and 2). After saline injection into the left antecubital vein, the coronary sinus filled first then emptied into the right atrium (RA). Also, after the injection of agitated saline into the right antecubital vein, there was rapid filling of the coronary sinus structure then emptying into the RA (Figure 3). After both injections, there was a moderate amount of saline contrast going across the atrial septum into the left atrium and left ventricle, raising the possibility of coexisting patent foramen ovale or atrial septal defect (Figure 4). All 4 pulmonary veins appeared to originate in the left atrium. The atrial septum appeared to be somewhat thin, but no definite atrial septal defect could be seen on the color flow study. Color flow study and Doppler revealed mild-moderate tricuspid regurgitation; the estimated systolic pulmonary pressure was 26 mm Hg. The estimated ejection fraction was 60%, without evidence of wall-motion abnormalities. There was no evidence of diastolic dysfunction,

A Rare Noncardiac Cause for Acute Myocardial Infarction in a 13-Year-Old Patient

A case of ST-segment elevation myocardial infarction in an adolescent patient is presented. The patient presented with resting angina and echocardiographic evidence of wall motion abnormalities in the inferior and posterior segments. The patient was known to have metastatic hepatocellular carcinoma. Tumor was seen in the left inferior pulmonary vein and is proposed to be the source of embolism-causing myocardial infarction. Secondary to intracranial metastatic lesions, the patient was treated conservatively with opiates, nitrates, and beta-blockers. This case is an opportunity to review the causes and management of myocardial infraction in pediatric patients and represents a rare cause of embolic myocardial infraction.

Complete reversal of ischemic wall motion abnormalities by combined use of gene therapy with transmyocardial laser revascularization

Introduction:Transmyocardial laser revascularization is believed to induce an angiogenic response within ischemic myocardium. We evaluated transgene expression in the setting of transmyocardial laser revascularization and hypothesized that intramyocardial injection of plasmid DNA encoding the gene for vascular endothelial growth factor could enhance the revascularization achieved by transmyocardial laser revascularization, resulting in improved cardiac function. Methods: Ten Yorkshire pigs had carbon dioxide–transmyocardial laser revascularization or acupuncture sites with injections of an expression plasmid encoding the gene for β-galactosidase with or without HVJ-liposomes. Three days after transduction, transgene expression was determined by enzyme-linked immunosorbent assay. Six weeks after placement of a constrictor on the left circumflex artery, 29 pigs were randomized to ischemic controls (n = 5), transmyocardial laser revascularization (n = 4), transmyocardial laser revascularization with expression plasmid β-galactosidase injections (n = 5), expression plasmid-vascular endothelial growth factor injections (n = 4), or transmyocardial laser revascularization with expression plasmid-vascular endothelial growth factor (n = 5) and harvested 6 weeks after therapy. Six transmyocardial laser revascularization pigs had either expression plasmid β-galactosidase or expression plasmid-vascular endothelial growth factor injections and were harvested at 2 weeks. Normal pigs (n = 5) were included for comparison. Left ventricular free wall motion was assessed by a cardiologist in a blinded manner. Results: Transgene expression did not vary significantly with or without HVJ-liposomes in transfected transmyocardial laser revascularization myocardium. However, expression was detected in 56 of 60 (93%) transmyocardial laser revascularization–transfected sites, but in only 10 of 20 (50%) non-transmyocardial laser revascularization sites ( P < .001). All (5 of 5 hearts) of the transmyocardial laser revascularization–vascular endothelial growth factor treated hearts displayed no evidence of wall motion abnormalities. Only these hearts had a statistically significantly different rate of wall motion abnormality compared with ischemic controls ( P = .004). Conclusion: Transfection efficiency was improved with the use of transmyocardial laser revascularization. Wall motion abnormalities were completely reversed within 6 weeks after transmyocardial laser revascularization with the direct injection of an expression plasmid encoding vascular endothelial growth factor. (J Thorac Cardiovasc Surg 1998;116:763-9)

Cardiac Trauma

Cardiac Trauma

Cardiac Ischemia During Weaning From Mechanical Ventilation

In this prospective study, we measured the ST segments, heart rate-systolic BP product (RPP), respiratory rate to tidal volume ratio (RVR), and pulse oximetry saturations of patients in our medical/cardiac ICUs before and during weaning from mechanical ventilation. Ninety-three patients were enrolled with a mean age of 66.5 +/- 15.0 years (mean +/- SD), mean acute physiology and chronic health evaluation (APACHE) II score of 16.0 +/- 6.9, and mean duration of mechanical ventilation of 5.2 +/- 8.6 days. Forty-nine patients had coronary artery disease (CAD). Six of 93 patients (6.4%) experienced ECG evidence of ischemia during weaning. Five of these six had a precedent history of CAD and four failed initial weaning attempts (22% of patients with CAD who failed weaning). The RPP, for the group as a whole, increased significantly during weaning from 12.0 +/- 3.1 to 13.4 +/- 4.0 mm Hg.bpm.10(3) (p<0.01). The rate to volume ratio did not change significantly during weaning, except in the subgroup of patients who failed to wean, in whom it increased from 98.4 +/- 45.2 to 124.9 +/- 54.9 bpm/L (p<0.05). Oxygenation also decreased significantly from 0.98 +/- 0.02 to 0.96 +/- 0.03 and was significantly associated with weaning failure (risk ratio [RR]=3.9; 95% confidence interval [CI]=1.7 to 9.0). Thirty-seven patients failed the initial weaning attempt. Cardiac ischemia (RR= 1.8; 95% CI=1.0 to 3.4) and an increased RVR (RR=1.7; 95% CI=0.9 to 3.4) tended to increase the risk of weaning failure. Cardiac ischemia, although infrequent (6%) in the general population of weaning medical/cardiac ICU patients, should be considered in patients with CAD who fail to wean.