Buccal caffeine strips for reversal of adverse symptoms of vasodilator stress.

BACKGROUND: Due to recurrent shortages of aminophylline, intravenous caffeine has emerged as a commonly used, safe and reliable method to treat adverse effects of vasodilator stress agents. We sought to evaluate the safety and effectiveness of buccal caffeine strips which are rapidly absorbed, inexpensive, readily available, and simplify caffeine administration. METHODS: Consecutive patients undergoing regadenoson stress SPECT MPI were assessed for the occurrence of symptoms during testing over an 11-week period at a single metropolitan hospital. Adverse symptoms, including their severity and duration, were recorded at the time of testing. Patient satisfaction was rated on a scale of 1 to 5 (5 being the most satisfied). Patients received reversal with caffeine if symptoms were felt to be significant enough by the patient and physician performing the test. The treatment received alternated week to week between IV caffeine (60 mg) or 100 mg buccal caffeine strips. Caffeine was given at least 3 minutes after tracer injection. A rescue dose of IV caffeine was offered 10 minutes later if indicated. RESULTS: Of the 122 patients enrolled in the study, 70 (57%) were included during buccal caffeine weeks and 52 (43%) during IV caffeine weeks, and only 28 (24%) received reversal with a caffeine agent. Seven (6%) received IV caffeine and 21 (17%) received buccal caffeine. There was no significant difference in symptom duration between IV and buccal caffeine after treatment (152.8 vs 163.4 seconds, P = 0.87). There was no significant difference in initial and final symptom severity between groups. Only 2 patients in the buccal group required rescue IV caffeine for ongoing symptoms and emesis. None of the IV group required a rescue dose. There was no significant difference in patient satisfaction between the groups (2.8 vs 3.2, P = 0.38). CONCLUSION: Buccal caffeine strips are a safe, well tolerated, and effective initial strategy to reverse adverse effects of vasodilator stress in the minority of patients who request it. Buccal caffeine alone or with IV rescue caffeine was highly effective in reversing adverse effects and was free of major adverse clinical events.

Human Platelets and Influenza Virus: Internalization and Platelet Activation.

Influenza infection has long been associated with prothrombotic outcomes in patients and platelets are the blood component predominantly responsible for thrombosis. In this review, we outline what is known about influenza interaction with human platelets, virion internalization, and viral RNA sensing, and the consequent impact on platelet function. We further discuss activation of platelets by IgG-influenza complexes and touch upon mechanisms of environmental platelet activation that relate to prothrombotic outcomes in patients during infection.

Comparative left ventricular mechanical deformation in acute apical variant stress cardiomyopathy and acute anterior myocardial infarction utilizing 2-dimensional longitudinal strain imaging.

AIMS: Despite three decades of study, it is still challenging to discriminate acute apical variant stress cardiomyopathy (AVSCM) from acute left anterior descending-myocardial infarction (LAD-MI) at the time of presentation. A biomarker or practical imaging modality that can differentiate these two entities is highly desirable. Our objective was to characterize left ventricular (LV) mechanical deformation using 2-dimensional (2D) echocardiographic strain imaging in an attempt to discriminate AVSCM from LAD-MI at presentation. METHODS AND RESULTS: We studied 108 women (60 AVSCM, 48 ST segment elevation LAD-MI). All underwent echocardiography within 48 hours of presentation. 2D longitudinal strain (LS) from an 18-segment LV model was performed, with global LS (GLS) taken as the average of all 18 segments. GLS was abnormal, but did not differentiate AVSCM from LAD-MI. Mean LS of the basal and mid-anterior, basal, and mid-anteroseptum segments were significantly lower in LAD-MI vs AVSCM group (-14 ± 9% vs -20 ± 8%; -11 ± 7% vs -14 ± 6%; -9 ± 8% vs -14 ± 8%; -9 ± 7% vs -13 ± 5%, respectively, all P ≤ .05). Mean LS of the basal inferior and inferolateral segments was significantly higher in the LAD-MI vs. AVSCM group (-19 ± 9% vs -13 ± 7%; -23 ± 11% vs -18 ± 7%, respectively, all P ≤ .05). Using ROC curve analysis, segmental strain ratio of average basal inferior and inferolateral segments LS to average mid- and basal anterior and anteroseptum segments LS of ≥1.58 was 90% specific for LAD-MI [area under the curve (AUC) 0.87; P < .001]. CONCLUSION: Longitudinal strain patterns are useful in discriminating AVSCM from LAD-MI patients at presentation and may be valuable in stratifying patients for invasive evaluation.

Activation of Inflammatory and Pro-Thrombotic Pathways in Acute Stress Cardiomyopathy.

Stress cardiomyopathy (SCM) is a unique cardiac disorder that more often occurs in women. SCM presents in a similar fashion as acute myocardial infarction (AMI), with chest pain, ECG changes, and congestive heart failure. The primary distinguishing feature is the absence of thrombotic coronary occlusion in SCM. How this reduction in cardiac function occurs in the absence of coronary occlusion remains unknown. Therefore, we tested the hypothesis that a targeted proteomic comparison of patients with acute SCM and AMI might identify relevant mechanistic differences. Blood was drawn in normal controls (n = 6), women with AMI (n = 12), or women with acute SCM (n = 15). Two-week follow-up samples were available in AMI (n = 4) and SCM patients (n = 11). Relative concentrations of 1,310 serum proteins were measured in each of the 48 samples using the SOMAscan assay. Women with AMI had greater myocyte necrosis, as reflected by a higher peak troponin I concentration (AMI 32.03 ± 29.46 vs. SCM 2.68 ± 2.6 ng/ml, p < 0.05). AMI and SCM patients had equivalent reductions in left ventricular ejection fraction [LVEF (%) 39 ± 12 vs. 37 ± 12, p = 0.479]. In follow-up, women with SCM had a greater improvement in cardiac function [LVEF (%) 60 ± 7 vs. 45 ± 13, p < 0.001]. No differentially expressed proteins were detected (absolute log2-fold change >1; q < 0.05) between AMI and SCM in the acute or recovery phase. However, when we compared normal controls to patients with AMI, there was differential expression of 35 proteins. When we compared normal controls to patients with SCM, 45 proteins were differentially expressed. In comparison to normal controls, biological processes such as complement, coagulation, and inflammation were activated in both AMI and SCM. There were four proteins that showed a non-significant trend to be increased in acute SCM vs. AMI (netrin-1, follistatin-like 3, kallikrein 7, kynureninase). Despite a lesser degree of myocardial necrosis than AMI, SCM is characterized by a similar activation of inflammatory, complement, and coagulation pathways. These findings may explain reported thromboembolic complications in the short term and elevated risk of mortality in the long term of SCM.