Alemtuzumab induced ST-segment elevation and acute myocardial dysfunction

AbstractCardiac toxicity as a side effect of chemotherapeutic agents has been well reported in the literature. Cardiac toxicity secondary to alemtuzumab has been reported, presenting as congestive heart failure and arrhythmias. Here we report a case of acute myocardial dysfunction after administration of a test dose of alemtuzumab. Our patient was a 66-year-old man with a history of small lymphocytic lymphoma/chronic lymphocytic lymphoma who received a test dose of alemtuzumab. Twenty minutes post administration, the patient developed nausea, vomiting, rigors, and tachycardia. Electrocardiography (ECG) showed acute ST-segment elevations in contiguous leads V2–V6, I, and AVL with no associated chest pain. Bedside echocardiogram showed akinesis of the anterior septum, apex, distal anterior wall, and decreased left ventricular ejection fraction. Cardiac catheterization showed non-critical occlusive disease and no intervention was undertaken. Post-catheterization ECG revealed resolution of ST segment elevations, TWI in V4–V6, and prolongation of corrected QT. Repeat echocardiogram 10 days after the event demonstrated no improvement in wall motion or ejection fraction. We discuss the possible mechanisms causing ST-elevations and acute myocardial dysfunction after treatment with alemtuzumab.<Learning objective: Alemtuzumab can cause acute myocardial dysfunction after administration of a test dose. Considering that this is a serious adverse effect, detailed cardiac evaluation and a high level of caution are recommended before administration of alemtuzumab. While no clear etiology could be identified for this side effect, excessive and acute cytokine release triggered by alemtuzumab administration is a possible explanation. This could be potentially attenuated by using anti-interleukin-6 or tumor necrosis factor inhibitors.

Prognostic significance of nonfatal reinfarction during 3-year follow-up: Results of the thrombolysis in myocardial infarction (TIMI) phase II clinical trial

Objectives.This study sought to assess the independent contribution of nonfatal reinfarction to the risk of subsequent death in patients with acute myocardial infarction undergoing thrombolytic therapy.Background.A composite of “unsatisfactory outcomes” as an end point has increased statistical power and facilitated evaluation of evolving treatment regimens in acute myocardial infarction. The significance of nonfatal reinfarction as a component of a composite end point has not been evaluated in the thrombolytic era.Methods.Event rate of nonfatal reinfarction over 3-year follow-up was evaluated in patients with acute myocardial infarction entered into the Thrombolysis in Myocardial Infarction Phase II trial. The independent risk of nonfatal reinfarction for subsequent death within various time intervals of follow-up was determined. The mortality rate after nonfatal reinfarction was compared with that of a matched control group.Results.During 3-year follow-up, 349 of 3,339 patients had a nonfatal reinfarction. Univariate predictors were history (antedating the index event) of angina (p = 0.01), hypertension (p = 0.01), multivessel disease (p = 0.007) and not a current smoker (p = 0.003); the latter was an independent predictor (relative risk [RR] 1.3, 99% confidence interval [CI]1.0 to 1.8). Forty-three of the 349 patients with a nonfatal reinfarction died: RR for death (vs. patients without a nonfatal reinfarction) was 1.9 (99% CI 1.1 to 3.2) if reinfarction occurred within 42 days of study entry, 6.2 (99% CI 3.0 to 12.9) if reinfarction occurred between 43 and 365 days and 2.9 (99% CI 0.6 to 13.4) if reinfarction occurred between 366 days and 3 years. The cumulative 3-year death rate was 14.1% in patients with a nonfatal reinfarction compared with 7.9% (p < 0.01) in a matched control group. Univariate predictors of death after nonfatal reinfarction were age ≥65 years (p < 0.001), not low risk category (p = 0.015) and history of heart failure before the index event (p < 0.001). Age ≥65 years was the only independent predictor (RR 5.4, 99% CI 2.3 to 12.4).Conclusions.Nonfatal reinfarction is a strong and independent predictor for subsequent death. It represents a powerful component for a composite end point in patients who received thrombolytic therapy after acute myocardial infarction

Cache valley virus in a patient diagnosed with aseptic meningitis

Cache Valley virus was initially isolated from mosquitoes and had been linked to central nervous system-associated diseases. A case of Cache Valley virus infection is described. The virus was cultured from a patient's cerebrospinal fluid and identified with real-time reverse transcription-PCR and sequencing, which also yielded the complete viral coding sequences

Myocardial Infarction in a Premenopausal Woman on Leuprolide Therapy

Premenopausal women with chest pain syndrome may have nonatherosclerotic coronary arteries with abnormal coronary flow. Estrogens have cardioprotective effect improving coronary vasodilatation. This case report discusses the consequences of leuprolide use by decreasing estrogen levels which led to acute myocardial infarction

Mild therapeutic hypothermia in patients resuscitated from out-of-hospital cardiac arrest: A meta-analysis of randomized controlled trials

Aims: Guidelines recommend mild therapeutic hypothermia (MTH) for survivors of out-of-hospital cardiac arrest (OHCA). However, there is little literature demonstrating a survival benefit. We performed a meta-analysis of randomized controlled trials (RCTs) assessing the efficacy of MTH in patients successfully resuscitated from OHCA. Materials and Methods: Electronic databases were searched for RCT involving MTH in survivors of OHCA, and the results were put through a meta-analysis. The primary endpoint was all-cause mortality, and the secondary endpoint was favorable neurological function. Odds ratios (ORs) and 95% confidence intervals (CIs) were computed using the Mantel-Haenszel method. A fixed-effect model was used and, if heterogeneity (I2 ) was >40, effects were analyzed using a random model. Results: Six RCT (n = 1400 patients) were included. Overall survival was 50.7%, and favorable neurological recovery was 45.5%. Pooled data demonstrated no significant all-cause mortality (OR, 0.81; 95% CI 0.55-1.21) or neurological recovery (OR, 0.77; 95% CI 0.47-1.24). No evidence of publication bias was observed. Conclusion: This meta-analysis demonstrated that MTH did not confer benefit on overall survival rate and neurological recovery in patients resuscitated from OHCA

Contemporary Sex-Based Differences by Age in Presenting Characteristics, Use of an Early Invasive Strategy, and Inhospital Mortality in Patients With Non-ST-Segment-Elevation Myocardial Infarction in the United States

BACKGROUND: Prior studies have reported higher inhospital mortality in women versus men with non-ST-segment-elevation myocardial infarction. Whether this is because of worse baseline risk profile compared with men or sex-based disparities in treatment is not completely understood. METHODS AND RESULTS: We queried the 2003 to 2014 National Inpatient Sample databases to identify all hospitalizations in patients aged \u3e/=18 years with the principal diagnosis of non-ST-segment-elevation myocardial infarction. Complex samples multivariable logistic regression models were used to examine sex differences in use of an early invasive strategy and inhospital mortality. Of 4 765 739 patients with non-ST-segment-elevation myocardial infarction, 2 026 285 (42.5%) were women. Women were on average 6 years older than men and had a higher comorbidity burden. Women were less likely to be treated with an early invasive strategy (29.4% versus 39.2%; adjusted odds ratio, 0.92; 95% confidence interval, 0.91-0.94). Women had higher crude inhospital mortality than men (4.7% versus 3.9%; unadjusted odds ratio, 1.22; 95% confidence interval, 1.20-1.25). After adjustment for age (adjusted odds ratio, 0.96; 95% confidence interval, 0.94-0.98) and additionally for comorbidities, other demographics, and hospital characteristics, women had 10% lower odds of inhospital mortality (adjusted odds ratio, 0.90; 95% confidence interval, 0.89-0.92). Further adjustment for differences in the use of an early invasive strategy did not change the association between female sex and lower risk-adjusted inhospital mortality. CONCLUSIONS: Although women were less likely to be treated with an early invasive strategy compared with men, the lower use of an early invasive strategy was not responsible for the higher crude inhospital mortality in women, which could be entirely explained by older age and higher comorbidity burden