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Primary percutaneous coronary intervention (PPCI) is the preferred treatment for acute ST segment elevation myocardial infarction (STEMI). The goal is reperfusion within 90 minutes of first medical contact (FMC) or 120 minutes if transfer is needed. Otherwise, fibrinolytic therapy is recommended. Mild therapeutic hypothermia (MTH) (≤35°C) before coronary reperfusion decreases myocardial infarct size. If applied before reperfusion, hypothermia could potentially lengthen the FMC-reperfusion time without increasing infarct size. Thirty-six swine had their mid left anterior descending coronary artery acutely occluded. All animals had an initial 30 minutes of occlusion to simulate typical delay before seeking medical attention. Eighteen animals were studied under normothermic conditions with reperfusion after an additional 40 minutes (the porcine equivalent of a 120-minute clinical FMC to reperfusion time) and 18 were treated with hypothermia but not reperfused until another 80 minutes (clinical equivalent of 240 minutes). Primary outcome was myocardial infarct size (infarct/area at risk [AAR]) at 24 hours. The two groups differed in systemic temperature at the time of reperfusion (39.1°C ± 1.0°C vs. 35.5°C ± 0.7°C; p  < 0.0001). Myocardial infarct size was not significantly different despite the longer time to reperfusion in those treated with hypothermia (60.6% ± 12% of the AAR [normothermic] vs. 65.8% ± 11.8% of the AAR [hypothermic]; p  = 0.39). Rapid induction of MTH during an anterior STEMI made it possible to extend the FMC to reperfusion time by the equivalent of an extra two clinical hours (120-240 minutes) without increasing the myocardial infarct size. This strategy could allow more STEMI patients to receive PPCI rather than the less effective intravenous fibrinolysis.

Objectives: The aim of this study was to test the hypothesis that hypothermia and early reperfusion are synergistic for limiting infarct size when an acutely occluded coronary is associated with cardiac arrest., Background: Cohort studies have shown that 1 in 4 post-cardiac arrest patients without ST-segment elevation has an acutely occluded coronary artery. However, many interventional cardiologists remain unconvinced that immediate coronary angiography is needed in these patients., Methods: Thirty-two swine (mean weight 35 ± 5 kg) were randomly assigned to 1 of the following 4 treatment groups: group A, hypothermia and reperfusion; group B, hypothermia and no reperfusion; group C, no hypothermia and reperfusion; and group D, no hypothermia and no reperfusion. The left anterior descending coronary artery was occluded with an intracoronary balloon, and ventricular fibrillation was electrically induced. Cardiopulmonary resuscitation was begun after 4 min of cardiac arrest. Defibrillation was attempted after 2 min of cardiopulmonary resuscitation. Resuscitated animals randomized to hypothermia were rapidly cooled to 34°C, whereas those randomized to reperfusion had such after 45 min of left anterior descending coronary artery occlusion., Results: At 4 h, myocardial infarct size was calculated. Group A had the smallest infarct size at 16.1 ± 19.6% (p < 0.05). Group C had an intermediate infarct size at 29.5 ± 20.2%, whereas groups B and D had the largest infarct sizes at 41.5 ± 15.5% and 41.1 ± 15.0%, respectively., Conclusions: Acute coronary occlusion is often associated with cardiac arrest, so treatment of resuscitated patients should include early coronary angiography for potential emergent reperfusion, while providing hypothermia for both brain and myocardial protection. Providing only early hypothermia, while delaying coronary angiography, is not optimal., (Copyright © 2016 American College of Cardiology Foundation. Published by Elsevier Inc. All rights reserved.)

Objectives: This study sought to determine whether "real-world" data supported the hypothesis that therapeutic hypothermia (TH) led to increased rates of stent thrombosis., Background: TH, which is often instituted after cardiac arrest (CA) to improve neurologic outcomes, alters pharmacokinetics of antiplatelet medications, leading to a theoretical risk of stent thrombosis after percutaneous coronary intervention (PCI)., Methods: CA patients with acute myocardial infarction undergoing PCI were identified from the Nationwide Inpatient Sample from 2006 to 2011, with a defined primary outcome of stent thrombosis. The incidence of stent thrombosis in patients undergoing TH versus those not undergoing TH was compared using both logistic regression and propensity score matching., Results: In this dataset, 49,109 CA patients underwent PCI for acute myocardial infarction from 2006 to 2011, of whom 1,193 (2.4%) underwent TH. The incidence of stent thrombosis in the TH group was 3.9% (43 of 1,193), compared to 4.7% (2,271 of 47,916) in the no TH group (p = 0.61). Logistic regression showed that TH was not a significant predictor of stent thrombosis with an adjusted odds ratio of 0.71 (95% confidence interval: 0.28 to 1.76; p = 0.46). Propensity matching was performed to adjust for baseline differences between the TH and no TH groups, matching 1,155 patients in the TH group with 3,399 patients in the no TH group. No difference was observed in the incidence of stent thrombosis in the TH and the no TH groups after propensity matching (3.5% vs. 6.1%; p = 0.17)., Conclusions: TH does not increase the incidence of stent thrombosis after primary PCI in patients with acute myocardial infarction presenting as CA., (Copyright © 2016 American College of Cardiology Foundation. Published by Elsevier Inc. All rights reserved.)

Targeted temperature management and early coronary angiography have become the standard of care for postcardiac arrest patients remaining comatose and with ST-segment elevation on the ECG. Less clear is the optimal approach for similar patients without ST-segment elevation on the postresuscitation ECG. However, current data from nonrandomized cohort studies suggest that many of these patients also benefit from an aggressive approach to postresuscitation care. Recent reports of increased stent thrombosis in the postarrest population need further exploration.

Objectives: The aim of this study was to compare outcomes and coronary angiographic findings in post-cardiac arrest patients with and without ST-segment elevation myocardial infarction (STEMI)., Background: The 2013 STEMI guidelines recommend performing immediate angiography in resuscitated patients whose initial electrocardiogram shows STEMI. The optimal approach for those without STEMI post-cardiac arrest is less clear., Methods: A retrospective evaluation of a post-cardiac arrest registry was performed., Results: The database consisted of 746 comatose post-cardiac arrest patients including 198 with STEMI (26.5%) and 548 without STEMI (73.5%). Overall survival was greater in those with STEMI compared with those without (55.1% vs. 41.3%; p = 0.001), whereas in all patients who underwent immediate coronary angiography, survival was similar between those with and without STEMI (54.7% vs. 57.9%; p = 0.60). A culprit vessel was more frequently identified in those with STEMI, but also in one-third of patients without STEMI (80.2% vs. 33.2%; p = 0.001). The majority of culprit vessels were occluded (STEMI, 92.7%; no STEMI, 69.2%; p < 0.0001). An occluded culprit vessel was found in 74.3% of STEMI patients and in 22.9% of no STEMI patients. Among cardiac arrest survivors discharged from the hospital who had presented without STEMI, coronary angiography was associated with better functional outcome (93.3% vs. 78.7%; p < 0.003)., Conclusions: Early coronary angiography is associated with improved functional outcome among resuscitated patients with and without STEMI. Resuscitated patients with a presumed cardiac etiology appear to benefit from immediate coronary angiography., (Copyright © 2015 American College of Cardiology Foundation. Published by Elsevier Inc. All rights reserved.)

Objectives: The aim of this study was to describe usage of the wearable cardioverter-defibrillator (WCD) during mandated waiting periods following myocardial infarction (MI) for patients perceived to be at high risk for sudden cardiac arrest (SCA)., Background: Current device guidelines and insurance coverage require waiting periods of either 40 days or 3 months before implanting a cardioverter-defibrillator post-myocardial infarction (MI), depending on whether or not acute revascularization was undertaken., Methods: We assessed characteristics of and outcomes for patients who had a WCD prescribed in the first 3 months post-MI. The WCD medical order registry was searched for patients who were coded as having had a "recent MI with ejection fraction ≤35%" or given an International Classification of Diseases, Ninth Revision 410.xx diagnostic code (acute MI), and then matched to device-recorded data., Results: Between September 2005 and July 2011, 8,453 unique patients (age 62.7 ± 12.7 years, 73% male) matched study criteria. A total of 133 patients (1.6%) received 309 appropriate shocks. Of these patients, 91% were resuscitated from a ventricular arrhythmia. For shocked patients, the left ventricular ejection fraction (LVEF) was ≤30% in 106, 30% to 35% in 17, >36% in 8, and not reported in 2 patients. Of the 38% of patients not revascularized, 84% had a LVEF ≤30%; of the 62% of patients revascularized, 77% had a LVEF ≤30%. The median time from the index MI to WCD therapy was 16 days. Of the treated patients, 75% received treatment in the first month, and 96% within the first 3 months of use. Shock success resulting in survival was 84% in nonrevascularized and 95% in revascularized patients., Conclusions: During the 40-day and 3-month waiting periods in patients post-MI, the WCD successfully treated SCA in 1.4%, and the risk was highest in the first month of WCD use. The WCD may benefit individual patients selected for high risk of SCA early post-MI., (Copyright © 2013 American College of Cardiology Foundation. Published by Elsevier Inc. All rights reserved.)

Background: In cardiac arrest, the ventricular fibrillation (VF) waveform, particularly amplitude spectral area (AMSA) and slope, predicts the return of spontaneous circulation (ROSC), but it is unknown whether the predictive utility differs in an acute myocardial infarction (MI), prior MI, or normal myocardium and if the waveform can distinguish the underlying myocardial state. We hypothesized that in a swine model of VF cardiac arrest, AMSA and slope predict ROSC after a shock independent of substrate and distinguish an acute from nonacute MI state., Methods and Results: MI was induced by occlusion of the left anterior descending artery. Post MI swine recovered for a 2-week period before induction of VF. VF was untreated for 8 minutes in 10 acute MI, 10 post MI, and 10 control swine. AMSA and slope predicted ROSC after a shock independent of myocardial state. For AMSA >31 mV-Hz, the odds ratio was 62 (P≤0.001) compared with AMSA <19 mV-Hz. For slope >3.1 mV/s, odds ratio was 52 (P≤0.001) compared with slope <1.8 mV/s. With chest compressions, AMSA and slope were significantly lower for acute MI swine compared with control swine, whereas in post MI swine the waveform characteristics were similar to control swine. In particular, for an AMSA >33.5 mV-Hz, the sensitivity to identify an acute from nonacute (control or post MI) state was 83%., Conclusions: In a swine model of VF cardiac arrest, AMSA and slope predict ROSC independent of myocardial substrate. Furthermore, with chest compressions, the VF waveform evolves differently and may offer a means to distinguish an acute MI.

Objective: We have demonstrated that a return of spontaneous circulation in the first 3 mins of resuscitation in swine is predicted by ventricular fibrillation waveform (amplitude spectral area or slope) when untreated ventricular fibrillation duration or presence of acute myocardial infarction is unknown. We hypothesized that in prolonged resuscitation efforts that return of spontaneous circulation immediately after a second or later shock with postshock chest compression is independently predicted by end-tidal CO2, coronary perfusion pressure, and ventricular fibrillation waveform measured before that shock in a swine model of ischemic and nonischemic ventricular fibrillation arrest., Design: Animal intervention study with comparison to a control group., Setting: University animal laboratory., Subjects: Twenty swine., Interventions: Myocardial infarction was induced by steel plug occlusion of the left anterior descending coronary artery. Ventricular fibrillation was untreated for 8 mins in normal swine (n=10) and acute myocardial infarction swine (n=10)., Measurements and Main Results: End-tidal CO2, coronary perfusion pressure, and ventricular fibrillation waveform characteristics of amplitude spectral area and slope were analyzed before second or later shocks. For an amplitude spectral area>35 mV-Hz, the odds ratio for achieving return of spontaneous circulation after that shock was 72 (95% confidence interval, 3.8-1300; p=.004) compared with an amplitude spectral area<28 mV-Hz and with an area under the receiver operator characteristic curve of 0.86. For slope>3.6 mV/s, the odds ratio for achieving return of spontaneous circulation was 36 (95% confidence interval, 2.7-480; p=.007) compared with slope<2.72 mV/s with an area under the curve of 0.86. End-tidal CO2 and coronary perfusion pressure were not predictive of return of spontaneous circulation after a shock, although coronary perfusion pressure was significantly related to both amplitude spectral area (p<.001) and slope (p<.001)., Conclusions: : In prolonged untreated ventricular fibrillation arrest, the waveform characteristics of amplitude spectral area and slope predict the attainment of return of spontaneous circulation with a second or later shock. This has implications for the ideal means to customize the timing of shocks and chest compressions when return of spontaneous circulation is not promptly obtained.

Introduction: Factors that affect resuscitation to a perfusing rhythm (ROSC) following ventricular fibrillation (VF) include untreated VF duration, acute myocardial infarction (AMI), and possibly factors reflected in the VF waveform. We hypothesized that resuscitation of VF to ROSC within 3min is predicted by the VF waveform, independent of untreated VF duration or presence of acute MI., Methods: AMI was induced by the occlusion of the left anterior descending coronary artery. VF was induced in normal (N=30) and AMI swine (N=30). Animals were resuscitated after untreated VF of brief (2min) or prolonged (8min) duration. VF waveform was analyzed before the first shock to compute the amplitude-spectral area (AMSA) and slope., Results: Unadjusted predictors of ROSC within 3min included untreated VF duration (8min vs 2min; OR 0.11, 95%CI 0.02-0.54), AMI (AMI vs normal; OR 0.11, 95%CI 0.02-0.54), AMSA (highest to lowest tertile; OR 15.5, 95%CI 1.7-140), and slope (highest to lowest tertile; OR 12.7, 95%CI 1.4-114). On multivariate regression, untreated VF duration (P=0.011) and AMI (P=0.003) predicted ROSC within 3min. Among secondary outcome variables, favorable neurological status at 24h was only predicted by VF duration (OR 0.22, 95% CI 0.05-0.92)., Conclusions: In this swine model of VF, untreated VF duration and AMI were independent predictors of ROSC following VF cardiac arrest. AMSA and slope predicted ROSC when VF duration or the presence of AMI were unknown. Importantly, the initial treatment of choice for short duration VF is defibrillation regardless of VF waveform.

Objective: In cardiac arrest resulting from ventricular fibrillation, the ventricular fibrillation waveform may be a clue to its duration and predict the likelihood of shock success. However, ventricular fibrillation occurs in different myocardial substrates such as ischemia, heart failure, and structurally normal hearts. We hypothesized that ventricular fibrillation is altered by myocardial infarction and varies from the acute to postmyocardial infarction periods., Design: An animal intervention study was conducted with comparison to a control group., Setting: This study took place in a university animal laboratory., Subjects: Study subjects included 37 swine., Interventions: Myocardial infarction was induced by occlusion of the midleft anterior descending artery. Ventricular fibrillation was induced in control swine, acute myocardial infarction swine, and in postmyocardial infarction swine after a 2-wk recovery period., Measurements and Main Results: Ventricular fibrillation was recorded in 11 swine with acute myocardial infarction, ten postmyocardial infarction, and 16 controls. Frequency (mean, median, dominant, and bandwidth) and amplitude-related content (slope, slope-amp [slope divided by amplitude], and amplitude-spectrum area) were analyzed. Frequencies at 5 mins of ventricular fibrillation were altered in both acute myocardial infarction (p < .001 for all frequency characteristics) and postmyocardial infarction swine (p = .015 for mean, .002 for median, .002 for dominant frequency, and <.001 for bandwidth). At 5 mins, median frequency was highest in controls, 10.9 +/- .4 Hz; lowest in acute myocardial infarction, 8.4 +/- .5 Hz; and intermediate in postmyocardial infarction, 9.7 +/- .5 Hz (p < .001 for acute myocardial infarction and p = .002 for postmyocardial infarction compared with control). Slope and amplitude-spectrum area were similar among the three groups with a shallow decline after minute 2, whereas slope-amp remained significantly altered for acute myocardial infarction swine at 5 mins (p = .003)., Conclusions: Ventricular fibrillation frequencies depend on myocardial substrate and evolve from the acute through healing phases of myocardial infarction. Amplitude related measures, however, are similar among these groups. It is unknown how defibrillation may be affected by relying on the ventricular fibrillation waveform without considering myocardial substrate.

Objective: Future automated external defibrillators are being designed to direct rescue efforts (chest compressions first vs. defibrillation) by inferring the duration of ventricular fibrillation based on its waveform characteristics such as frequency content. This approach assumes that the ventricular fibrillation waveform is an appropriate surrogate for ventricular fibrillation duration and is not affected by structural heart disease. We hypothesized that an acute myocardial infarction may alter the frequency content of ventricular fibrillation., Design: Animal intervention study with comparison to control group., Setting: University animal laboratory., Subjects: Twenty-seven swine., Interventions: Acute myocardial infarction was induced by occlusion of the mid-left anterior descending artery. Ventricular fibrillation was induced in swine with acute myocardial infarction and control swine., Measurements and Main Results: Ventricular fibrillation was induced in 11 swine with an acute myocardial infarction and in 16 control swine. Ventricular fibrillation waveforms were analyzed for mean, median, and dominant frequency, as well as bandwidth and amplitude. All frequency characteristics were significantly (p < .001) altered in swine with acute myocardial infarction compared with controls. Specifically, these characteristics were significantly depressed and varied little over time in swine with acute myocardial infarction compared with controls., Conclusions: These data establish that ventricular fibrillation during an acute myocardial infarction has an altered frequency content and time evolution compared with ventricular fibrillation without coronary obstruction. Frequency characteristics such as mean, median, dominant, and bandwidth show little variation in time after an acute myocardial infarction and are not suitable surrogates for ventricular fibrillation duration. These findings have important implications for the development of "smart" automated external defibrillators designed to determine duration of ventricular fibrillation from the waveform characteristics.

Background: For prolonged VF, perfusion of the myocardium by pre-shock chest compressions can improve myocardial readiness for successful defibrillation. Characteristics of the VF waveform correlate with the duration of VF when there is no structural heart disease. A "smart" automated external defibrillator (AED) could therefore analyze the VF waveform, determine if VF has been prolonged, and then direct rescuers to either deliver a shock first or chest compressions first. We hypothesized that ischemic heart failure might alter the waveform content of ventricular fibrillation compared with normal hearts, complicating the determination of VF duration., Methods: Myocardial infarction was induced by ligating the proximal left coronary artery. Six weeks later, VF was then induced in 10 rats with myocardial infarction and heart failure (MI-CHF) and 9 control rats. Waveforms were analyzed for total signal amplitude, median frequency, dominant frequency and bandwidth (the frequency interval containing 50% of the total amplitude about the median frequency)., Results: All of these VF waveform characteristics were altered substantially in MI-CHF rats compared to normal controls. In particular, MI-CHF rats had decreased signal amplitude early in VF (p=0.02), a broader bandwidth (p=0.001) and different frequency characteristics over time (p<0.001)., Conclusions: VF waveforms vary over time in a typical manner among rats with and without ischemic heart failure. However, the time-course and waveform characteristics of ventricular fibrillation are altered in rats with myocardial infarctions and ischemic heart failure compared to normal controls. These findings have important implications regarding the use of waveform analyses to determine the duration of VF.

Despite substantial progress in the diagnosis and treatment of acute ST-segment elevation myocardial infarction (STEMI), implementation of this knowledge into routine clinical practice has been variable. It has become increasing clear that primary percutaneous coronary intervention (PCI) is the preferred method of reperfusion if it can be performed in a timely manner. Recent European data suggest that transfer for direct PCI may also be preferable to fibrinolytic therapy. We believe it is time to establish a national policy for treatment of patients with STEMI to develop a coordinated system of care similar to that of the level 1 trauma system.

The acute coronary syndromes (ACS) represent a heterogeneous group of patients along a continuum of risk from unstable angina to non-ST-segment elevation myocardial infarction. ACS is a term that has been used to describe the constellation of clinical symptoms that represent acute myocardial ischemia. This article reviews the adjunctive medications that are used during emergency cardiovasculare care for the early management of patients experiencing the ACS. The adjunctive therapies are divided into early immediate treatment and then subsequent management in the acute care setting.

Background: Mouth-to-mouth rescue breathing is a barrier to the performance of bystander cardiopulmonary resuscitation (CPR). We evaluated the need for assisted ventilation during simulated single-rescuer bystander CPR in a swine myocardial infarction model of prehospital cardiac arrest., Methods and Results: Steel cylinders were placed in the mid left anterior descending coronary arteries of 43 swine. Two minutes after ventricular fibrillation, animals were randomly assigned to 10 minutes of hand-bag-valve ventilation with 17% oxygen and 4% carbon dioxide plus chest compressions (CC+V), chest compressions only (CC), or no CPR (control group). Standard advanced life support was then provided. Animals successfully resuscitated received 1 hour of intensive care support and were observed for 24 hours. Five of 14 CC animals, 3 of 15 CC+V animals, and 1 of 14 controls survived for 24 hours (CC versus controls, P=.07). Myocardial oxygen delivery and consumption were greater among surviving animals than nonsurvivors but did not differ between CC and CC+V animals., Conclusions: In this acute myocardial infarction model of prehospital single-rescuer bystander CPR, assisted ventilation did not improve outcome.

The usefulness of intravenous beta-adrenergic receptor blockade in limiting infarct size when neither reperfusion nor collateral flow occurs is unknown. The effect of intravenous metoprolol on limiting myocardial infarct size was therefore examined in a nonreperfused porcine model. Closed-chest techniques were used to occlude the left anterior descending coronary artery, after which animals were randomized at 20 minutes to receive intravenous metoprolol, 0.75 mg/kg, or placebo. Infarct size examined at 5 hours with Evans blue and triphenyltetrazolium staining techniques was expressed as a percentage of total ventricular myocardium at ischemic risk. This percentage was not significantly different between the groups (84% +/- 5% with metoprolol vs 90% +/- 4% with placebo; p = 0.4). Myocardial infarct size was not significantly decreased at 5 hours by early administration of intravenous metoprolol when the infarct artery remained occluded and collateral flow was minimal.

A retrospective review was conducted to determine the incidence of cardiac catheterization for postinfarction angina, the associated coronary anatomy, and the subsequent clinical course. Over one year, 30 of 178 myocardial infarctions were complicated by postinfarction angina resulting in cardiac catheterization. This was 18% of cardiac catheterizations for evaluation of coronary artery disease. Among the 30 patients, 3 had left main disease, 3 had triple-vessel disease, 11 had double-vessel disease, 11 had single-vessel disease, and 2 had no significant disease. Nine patients had proximal left anterior descending disease without left main disease. In contrast to previous autopsy or surgical series, the extent of coronary artery involvement was less severe and followed a distribution similar to that found in uncomplicated myocardial infarctions. Nevertheless, 17 of the 30 patients underwent revascularization with angioplasty or bypass surgery compared with 41 of 137 without postinfarction angina (p = 0.01). Clinical characteristics of the patients with postinfarction angina did not predict who would ultimately require revascularization. Cardiac catheterization is necessary for management of patients with postinfarction angina, because a majority of them will require revascularization.

To determine the effect of an anteroseptal myocardial infarction on right ventricular systolic and diastolic function, we studied 12 pigs before and 1 h after left anterior descending coronary artery occlusion. Total arterial occlusion was achieved by the percutaneous, transcatheter placement of a 1 mm Teflon plug into the mid portion of the artery. The resulting infarction involved 28 (SEM 3)% of the left ventricular wall, in the anterior and septal regions. A small rim of the right ventricular free wall adjacent to the septum and the right ventricular apex were also affected. End diastolic pressures in both ventricles rose significantly: left ventricular from 12(1) to 20(2) mm Hg and right ventricular from 8(1) to 10(1) mm Hg. Right ventricular peak systolic pressure increased from 29(2) to 35(2) mm Hg while left ventricular peak systolic pressure did not change. One hour after infarction the half time of isovolumic relaxation of the right ventricle was prolonged from 6.9(0.5) to 8.7(0.4) ms. Ejection fraction in both ventricles was depressed: from 46(1) to 34(2)% in the right ventricle and from 69(3) to 49(3) in the left ventricle. There was no change in either right or left ventricular dP/dt. These data suggest that right ventricular systolic and diastolic dysfunction occurs as the result of an anteroseptal myocardial infarction in pigs.