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Atrial fibrillation (AF), the most common form of dysrhythmia, steadily increases in prevalence with age. If left untreated, AF significantly increases the risk of stroke, heart failure, and death. Despite the increasing prevalence, there are significant research gaps in the prediagnosis symptom experiences of patients with AF.The purpose of this qualitative descriptive study was to explore the prediagnosis symptom experience of patients with AF.Participants 19 years or older with AF diagnosed in the previous year were recruited (n = 26) from outpatient cardiac rehabilitation and AF clinics. Semistructured interviews, broadly guided by the Symptom Experience Model, explored perceptions, evaluations, and responses to AF symptoms. Thematic analysis used a 2-step approach, deductively coding for participants' symptom perceptions, evaluations, and responses and inductively coding within these broader Symptom Experience Model concepts.Perception involved awareness of bodily sensations, ranging from imperceptible noticing to commanding attention, heightened by rest and activity. In evaluation, participants used self-derived theories to explain their symptoms, gathered evidence to support/refute their theories, and formulated alternative theories as symptoms changed over time. Responses consisted of nontreatment, self-treatment, and health seeking; most participants needed repeated healthcare visits before diagnosis.The current study identified challenges participants experienced in developing awareness of their AF symptoms, the complex cognitive processes associated with evaluation, and barriers that made it difficult to respond to AF symptoms in a timely manner. Understanding the prediagnosis symptom experience from the patient's perspective is essential for the enhancement of current AF screening practices.

With the number of heart transplants being performed each year stagnating due to lack of donors the left ventricular assist device (LVAD) patient population will continue to grow. As more and more patients are living longer with LVADs, either as a bridge to transplant or destination therapy, we will continue to see an increased number of complications related to assist device therapy. One of the common challenges physicians face are patients who suffer from both bleeding and thrombotic complications. When bleeding complications occur anticoagulation is usually reduced or discontinued and then the thrombosis risk increases. Once a pump thrombosis occurs there are limited percutaneous treatment strategies available, especially in the setting of a recent bleeding event. Surgical exchange is the only definitive therapy and that can be a high risk and difficult operation. Turning off an LVAD may become necessary, as it did in our case, but that can lead to significant retrograde flow through the device and rapid patient decline. A prompt percutaneous therapy is needed to stabilize these patients.

BACKGROUND: High-degree AV block (HDAVB) is a known complication after both transcatheter aortic valve implantation (TAVI) and surgical aortic valve replacement (SAVR). Data about the contemporary practice pattern of permanent pacing, especially the timing of implantation, for HDAVB after TAVI compared to SAVR are limited. METHODS: Using the National Inpatient Sample database, we identified patients who underwent TAVI or SAVR from 2012 to 2014. We excluded patients with a prior pacemaker and implantable cardioverter defibrillator. The incidence of HDAVB, the rate of permanent pacemaker implantation and its timing were compared between TAVI and SAVR groups. RESULTS: We identified 33,690 and 202,110 patients who underwent TAVI and SAVR, respectively. HDAVB occurred in 3,480 patients (10.3%) in the TAVI group and 11,405 patients (5.6%) in the SAVR group (p

Patients with diabetes mellitus (DM) have increased propensity to generate thromboxane A2 (TXA2) and other eicosanoids which can contribute to their heightened platelet reactivity. EV-077 is a potent thromboxane receptor antagonist and thromboxane synthase inhibitor and thus represents an attractive therapy in patients with DM. However, the effects of EV-077 on pharmacodynamic (PD) profiles in patients with DM and coronary artery disease (CAD) while on antiplatelet therapy is poorly explored and represented the aim of this in vitro pilot investigation. Patients with DM and stable CAD (n = 10) on low-dose aspirin (81 mg/day) were enrolled and then switched to clopidogrel (75 mg/day) monotherapy for 7-10 days. PD assessments were conducted while on aspirin and on clopidogrel using light transmittance aggregometry following stimuli with U-46619 [TXA2 stable analogue (7 μM)], arachidonic acid [AA (1 mM)], collagen (3 μg/mL) and adenosine diphosphate [ADP (5 μM and 20 μM)] with and without in vitro EV-077. EV-077 completely inhibited U-46619-stimulated platelet aggregation (p = 0.005 for both aspirin and clopidogrel) and also showed a significant reduction of collagen-induced aggregation (aspirin p = 0.008; clopidogrel p = 0.005). EV-077 significantly reduced AA-induced platelet aggregation in clopidogrel (p = 0.009), but not aspirin (p = 0.667) treated patients. Ultimately, EV-077 significantly reduced ADP-mediated platelet aggregation in both aspirin (ADP 5 μM p = 0.012; ADP 20 μM p = 0.032) and clopidogrel (ADP 5 μM p = 0.007; ADP 20 μM p = 0.008) treated patients. In conclusion, in DM patients with CAD on aspirin or clopidogrel monotherapy, in vitro EV-077 exerts potent platelet inhibitory effects on multiple platelet signaling pathways. These data support that EV-077 has only additive platelet inhibiting effects on top of standard antiplatelet therapies. These findings warrant further investigation in ex vivo settings.

ST-elevation myocardial infarction (STEMI) identification by emergency medicine services (EMS) leading to pre-hospital catheterization laboratory (CL) activation shortens ischemic time and improves outcomes. We examined the incremental value of addition of a screening clinical tool (CT), containing clinical information and a Zoll electrocardiogram (ECG)-resident STEMI identification program (ZI) to ZI alone.All EMS-performed and ZI-analyzed ECGs transmitted to a percutaneous coronary intervention hospital from October 2009 to January 2011 were reviewed for diagnostic accuracy. ZI performance was also compared to ECG interpretations by 2 experienced readers The CT was then retrospectively applied to determine the incremental benefit above the ZI alone.ST-elevation myocardial infarction was confirmed in 23 (7.5%) of 305 patients. ZI was positive in 37 (12.1%): sensitivity: 95.6% and specificity: 94.6%, positive predictive value (PPV), 59.5%, negative predictive value (NPV), 99.6%, and accuracy of 93.8%. Moderate agreement was observed among the readers and ZI. CT criteria for CL activation were met in 24 (7.8%): 20 (83.3%) were confirmed STEMIs: sensitivity: 86.9%, specificity: 98.5%, a PPV: 83.3%, and NPV: 98.6%, accuracy of 97.7%. CT + ZI increased PPV (P0.05) and specificity (P0.003) by reducing false positive STEMI identifications from 15 (4.9%) to 4 (1.3%).In an urban cohort of all EMS transmitted ECGs, ZI has high sensitivity and specificity for STEMI identification. Whereas the PPV was low, reflecting both low STEMI prevalence and presence of STEMI-mimics, the NPV was very high. These findings suggest that a simplified CT combined with computer STEMI interpretation can identify patients for pre-hospital CL activation. Confirmation of these results could improve the design of STEMI care systems.

SummaryDifferent aspirin dosing regimens have been suggested to impact outcomes when used in combination with adenosine diphosphate (ADP) P2Y12 receptor antagonists. Prior investigations have shown that not only aspirin, but also potent ADP P2Y12 receptor blockade can inhibit thromboxane A2-mediated platelet activation. The impact of aspirin dosing on ADP mediated platelet activities is unknown and represents the aim of this in vitro pilot pharmacodynamic (PD) investigation. Twenty-six patients with stable coronary artery disease on aspirin 81 mg/day and P2Y12 naïve were enrolled. PD assessments were performed at baseline, while patients were on 81 mg/day aspirin and after switching to 325 mg/day for 7 ± 2 days with and without escalating concentrations (vehicle, 1, 3, and 10 μM) of prasugrel’s active metabolite (P-AM). PD assays included flow cytometric assessment of VASP to define the platelet reactivity index (PRI) and the Multiplate Analyzer (MEA) using multiple agonists [ADP, ADP + prostaglandin (PGE1), arachidonic acid (AA), and collagen]. Escalating P-AM concentrations showed incremental platelet P2Y12 inhibition measured by VASP-PRI (p

Despite the frequency and long duration of aspirin use, its role in primary and secondary prevention in older adults is not well studied. This review takes a critical look at the available literature on aspirin efficacy in elderly adults, and some relevant guidelines for practicing physicians are suggested.

Pharmacodynamic (PD) studies comparing prasugrel and ticagrelor have reached inconsistent findings. Therefore, a comprehensive investigation comparing the PD effects of prasugrel vs. ticagrelor after switching from clopidogrel therapy, exploring both loading dose (LD) and maintenance dose (MD) regimens represented the aim of this study.Patients (n = 110) with coronary artery disease were randomized to prasugrel (60 mg LD/10 mg MD q.d.) or ticagrelor (180 mg LD/90 mg MD b.i.d) therapy for 1 week. Pharmacodynamic assessments were conducted using three assays (vasodilator-stimulated phosphoprotein, VerifyNow P2Y12, and light transmittance aggregometry, LTA) at baseline, 30 min, 2, 24 h, and 1 week. The impact of initiating ticagrelor MD 12 vs. 24 h after LD administration was also assessed. Switching clopidogrel-treated patients to an LD of prasugrel or ticagrelor was associated with a reduction in platelet reactivity at 30 min and was sustained at all time points up to 1 week with the MD (P0.001 for all assays). Platelet reactivity was similar with prasugrel and ticagrelor with all assays at 30 min, 2 h, and 1 week (P0.05 for all time points), with the exception of LTA at 30 min (lower with prasugrel; P = 0.003). At 24 h, platelet reactivity was lower among patients initiating ticagrelor MD after 12 vs. 24 h post-LD. Rates of high platelet reactivity (HPR) were markedly reduced and similar between groups.Prasugrel and ticagrelor exert similar levels of P2Y12 inhibition achieving more potent PD effects and reduced HPR rates compared with clopidogrel which are reached promptly following LD and sustained with MD.NCT01852175.

Objectives: We reviewed data to validate the use of a simplified STEMI Alert Clinical Tool for EMS personnel to use to activate cardiac cath labs for patients presenting with STEMIs. Methods: We retrospectively reviewed all ECGs transmitted by one EMS provider to an urban primary PCI facility from October 2009 to January 2011. We then applied the STEMI Alert Clinical Tool (Table 1) to determine if the patient would have qualified for cath lab activation from the field. A retrospective chart review was performed to determine the outcomes of each transmission within the corresponding time frames. Results: A total of 307 ECGs were transmitted during the selected time frame. A total of 10.7% (33 of 307) met criteria for cath lab activation based on the STEMI alert clinical tool. Of these 63.6% (21 of 33) were true positives and 36.4% (12 of 33) were false positives. The sensitivity of a positive alert was 95.5% (21 of 22) and the specificity was 95.8% (273 of 285). The positive predictive value (PPV) was 63.6% (21 of 33). One STEMI patient was missed by the clinical tool because the ECG did not read ***ACUTE MI***. The negative predictive value (NPV) was 99.6% (273 of 274). Conclusions: The data from this study shows that use of a STEMI Alert Clinical Tool has a relatively low PPV but a very high NPV. Thus, pre-hospital activation of cath labs may not be necessary for patients who fail to meet the STEMI alert criteria. In contrast, despite use of this tool a portion of patients will falsely activate the cath lab. Although this strategy may increase the risks of unnecessary financial and man power utilization to the hospital system, the risk of missing a STEMI can be high. Analyzing a larger patient population will be required to further define the value of using this clinical tool. Table 1 - Clinical Tool - All 7 must be "yes" to activate cath lab

Background: Rapid reperfusion of ST elevation myocardial infarction (STEMI) patients with primary percutaneous coronary intervention (PCI) improves outcomes. Systems have been developed in many areas to identify STEMI patients in the field using pre-hospital electrocardiograms (ECGs). The Zoll E-Series (ES) is a defibrillator/monitoring system that utilizes the GE Medical Systems 12SL interpretive algorithm to assist with identification of STEMIs. There is a lack of significant data measuring the accuracy of the Zoll ES and its algorithm, especially in the setting of a large urban population. Methods: We retrospectively looked at 307 consecutive ECGs transmitted by one emergency medical service (EMS) provider to an urban primary PCI facility from October 2009 to January 2011. All transmissions were from Zoll ES monitors. Multiple ECG computer interpretations were screened and filtered out to those labeled ***ACUTE MI***. A retrospective chart review was performed to determine the clinical outcome for each transmission in order to determine the performance of the interpretive algorithm in this population. Results: Overall, 307 ECGs were analyzed. A total of 7% (20 of 307) were confirmed STEMIs (Table 1). The computer reading shows a sensitivity of 95% (20 of 21) and specificity of 94% (268 of 286). There is a positive predictive value (PPV) of 53% (20 of 38). Conclusions: The initial data from this study shows that the Zoll ES has a remarkably high sensitivity of 95% but a poor PPV of 53%. This may be due to multiple confounders that result in STEMI “mimics.” The Zoll ES helps provide a pre-hospital ECG that serves as a powerful and life saving tool in the field. However, due to the low PPV, these findings reinforce that the pre-hospital ECG needs to be combined with an appropriate clinical history and additional human interpretation. Further studies analyzing a larger population of patients should be conducted to further assess the value of using this tool.

The intentional consumption and use of stimulants, such as caffeine, are known to have numerous interactions with the human cardiovascular system. Ex vivo studies have shown caffeine-induced vasoconstriction of coronary arteries (Forman et al. in Ann Emerg Med 29:178-180, 1997). We report on a case of a 17-year-old male who presented with angina and an abnormal electrocardiogram (ECG) concerning for ST elevation myocardial infarct. He was found to have diffuse ECG changes and markedly elevated cardiac enzymes. A transthoracic echocardiogram revealed a reduced left ventricular (LV) systolic function as well as segmental wall motion abnormalities consistent with an ischemic insult. The patient admitted to consuming near lethal doses of caffeine immediately preceding his angina. He was diagnosed with coronary vasospasms as a result of stimulant use. During hospitalization, ECG changes resolved, cardiac enzymes started trending downward, and LV systolic function returned to normal, all consistent with stunned myocardium that fully recovered. This case strongly suggests that overuse of stimulants, such as caffeine, should be considered in patients presenting with coronary vasospasms, particularly in teenagers and young adults.

Diabetes mellitus (DM) patients have increased thromboxane A2 (TXA2) which activate TX prostanoid receptors (TPR). In DM patients, EV–077, a combined TXA2 synthase inhibitor and TPR antagonist, achieves more effective platelet inhibition compared with aspirin. However, the effects of EV–077 in