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Aim This clinical practice guideline for the evaluation and diagnosis of chest pain provides recommendations and algorithms for clinicians to assess and diagnose chest pain in adult patients. Methods A comprehensive literature search was conducted from November 11, 2017, to May 1, 2020, encompassing randomized and nonrandomized trials, observational studies, registries, reviews, and other evidence conducted on human subjects that were published in English from PubMed, EMBASE, the Cochrane Collaboration, Agency for Healthcare Research and Quality reports, and other relevant databases. Additional relevant studies, published through April 2021, were also considered. Structure Chest pain is a frequent cause for emergency department visits in the United States. The “2021 AHA/ACC/ASE/CHEST/SAEM/SCCT/SCMR Guideline for the Evaluation and Diagnosis of Chest Pain” provides recommendations based on contemporary evidence on the assessment and evaluation of chest pain. This guideline presents an evidence-based approach to risk stratification and the diagnostic workup for the evaluation of chest pain. Cost-value considerations in diagnostic testing have been incorporated, and shared decision-making with patients is recommended.

Aim This executive summary of the hypertrophic cardiomyopathy clinical practice guideline provides recommendations and algorithms for clinicians to diagnose and manage hypertrophic cardiomyopathy in adult and pediatric patients as well as supporting documentation to encourage their use. Methods A comprehensive literature search was conducted from January 1, 2010, to April 30, 2020, encompassing studies, reviews, and other evidence conducted on human subjects that were published in English from PubMed, EMBASE, the Cochrane Collaboration, Agency for Healthcare Research and Quality reports, and other relevant databases. Structure Many recommendations from the earlier hypertrophic cardiomyopathy guidelines have been updated with new evidence or a better understanding of earlier evidence. This summary operationalizes the recommendations from the full guideline and presents a combination of diagnostic work-up, genetic and family screening, risk stratification approaches, lifestyle modifications, surgical and catheter interventions, and medications that constitute components of guideline directed medical therapy. For both guideline-directed medical therapy and other recommended drug treatment regimens, the reader is advised to follow dosing, contraindications and drug-drug interactions based on product insert materials.

Transvenous neurostimulation of the phrenic nerve (PNS) is a potentially improved and unique approach to the treatment of central sleep apnea (CSA). There have been multiple studies with limited individuals evaluating the efficacy of PNS. Our aim was to review and pool those studies to better understand whether phrenic nerve stimulation is efficacious in the treatment of CSA. The initial search on Pubmed retrieved a total of 97 articles and after screening all articles, only 5 could be included in our quantitative analysis. Pooling of data from 5 studies with a total of 204 patients demonstrated a reduction of mean apnea hypopnea index with PNS compared to controls by -26.7 events/hour with 95% confidence interval and P value of [CI (-31.99, -21.46), I2 85, p 0.00]. The mean difference in central apnea index was -22.47 [CI (-25.19, -19.76), I2 0, p 0.00]. The mean reduction in the oxygen desaturation index of 4% or more demonstrated a decrease in PNS group by -24.16 events/hour [(CI -26.20, -22.12), I2 0, p 0.00] compared with controls. PNS resulted in mean reduction in arousal index of -13.77 [CI (-16.15, -11.40), I2 0, p 0.00]. The mean change in percent of time spent in rapid eye movement sleep demonstrated a nonsignificant increase in PNS group by 1.01 % [CI (-5.67, 7.86), I293, p 0.75]. In conclusion, PNS therapy for treating CSA demonstrated positive outcomes but larger randomized studies are needed to evaluate the safety and clinical outcomes.

Glenn N. Levine, MD, FACC, FAHA, Chair Patrick T. O’Gara, MD, MACC, FAHA, Chair-Elect Jonathan L. Halperin, MD, FACC, FAHA, Immediate Past Chair [‡‡][1] Sana M. Al-Khatib, MD, MHS, FACC, FAHA Joshua A. Beckman, MD, MS, FAHA Kim K. Birtcher, PharmD, MS, AACC Biykem Bozkurt, MD, PhD

Since 1980, the American College of Cardiology (ACC) and American Heart Association (AHA) have translated scientific evidence into clinical practice guidelines with recommendations to improve cardiovascular health [(1)][1]. These guidelines, based on systematic methods to evaluate and classify

Glenn N. Levine, MD, FACC, FAHA, Chair Patrick T. O’Gara, MD, MACC, FAHA, Chair-Elect Jonathan L. Halperin, MD, FACC, FAHA, Immediate Past Chair [¶][1] Sana M. Al-Khatib, MD, MHS, FACC, FAHA Joshua A. Beckman, MD, MS, FAHA Kim K. Birtcher, MS, PharmD, AACC Biykem Bozkurt, MD, PhD, FACC

Glenn N. Levine, MD, FACC, FAHA, Chair Patrick T. O’Gara, MD, MACC, FAHA, Chair-Elect Jonathan L. Halperin, MD, FACC, FAHA, Immediate Past Chair [¶][1] Sana M. Al-Khatib, MD, MHS, FACC, FAHA Joshua A. Beckman, MD, MS, FAHA Kim K. Birtcher, MS, PharmD, AACC Biykem Bozkurt, MD, PhD, FACC

Objective To review the literature systematically to determine whether noninvasive or invasive risk stratification, such as with an electrophysiological study of patients with asymptomatic pre-excitation, reduces the risk of arrhythmic events and improves patient outcomes. Methods PubMed, EMBASE, and the Cochrane Central Register of Controlled Trials (all January 1, 1970, through August 31, 2014) were searched for randomized controlled trials and cohort studies examining noninvasive or invasive risk stratification in patients with asymptomatic pre-excitation. Studies were rejected for low-quality design or the lack of an outcome, population, intervention, or comparator of interest or if they were written in a language other than English. Results Of 778 citations found, 9 studies met all the eligibility criteria and were included in this paper. Of the 9 studies, 1 had a dual design–a randomized controlled trial of ablation versus no ablation in 76 patients and an uncontrolled prospective cohort of 148 additional patients–and 8 were uncontrolled prospective cohort studies (n=1,594). In studies reporting a mean age, the range was 32 to 50 years, and in studies reporting a median age, the range was 19 to 36 years. The majority of patients were male (range, 50% to 74%), and 250 ms) developed in 0% to 16%, malignant atrial fibrillation (shortest RR interval ≤250 ms) in 0% to 9%, and ventricular fibrillation in 0% to 2%, most of whom were children in the last case. Conclusions The existing evidence suggests risk stratification with an electrophysiological study of patients with asymptomatic pre-excitation may be beneficial, along with consideration of accessory-pathway ablation in those deemed to be at high risk of future arrhythmias. Given the limitations of the existing data, well-designed and well-conducted studies are needed.

Preamble e472 1. Introduction e473 2. General Principles e475 3. Sinus Tachyarrhythmias e480 4. Nonsinus Focal Atrial Tachycardia and MAT e481 5. Atrioventricular Nodal Reentrant Tachycardia e482 6. Manifest and Concealed Accessory Pathways e483 7. Atrial Flutter e485 8. Junctional Tachycardia e487 9. Special Populations e487

Jonathan L. Halperin, MD, FACC, FAHA, Chair Glenn N. Levine, MD, FACC, FAHA, Chair-Elect Jeffrey L. Anderson, MD, FACC, FAHA, Immediate Past Chair [¶][1] Nancy M. Albert, PhD, RN, FAHA[¶][1] Sana M. Al-Khatib, MD, MHS, FACC, FAHA Kim K. Birtcher, PharmD, AACC Biykem Bozkurt, MD, PhD, FACC

Risk stratification for patients with an asymptomatic Wolff-Parkinson-White (WPW) electrocardiogram (ECG) pattern remains an area of controversy. A 33 year old man with a known history of WPW ECG pattern without prior symptoms presented to the emergency room with palpitations that occurred moments

This study assesses the effect of biventricular pacing on sympathetic nerve activity (SNA) in patients with depressed ejection fraction and intraventricular conduction delay (IVCD). Biventricular pacing has been shown to result in hemodynamic improvement in patients with depressed ejection fraction and IVCD. The effect of biventricular pacing on SNA, however, remains unclear. A total of 15 men with a mean ejection fraction of 25 +/- 4% were enrolled. Arterial pressure, central venous pressure and SNA were recorded during 3 minutes of right atrial (RA) pacing and RA-biventricular pacing. Pacing was performed at a rate 5 to 10 beats faster than sinus rhythm, with an atrioventricular interval equal to 100 ms during RA-biventricular pacing. RA-biventricular pacing resulted in greater arterial pressures (p0.05) than RA pacing (146 +/- 15/83 +/- 11 vs 141 +/- 15/80 +/- 10 mm Hg). There were no differences in central venous pressures between the 2 pacing modes (p = 0.76). SNA was significantly less during RA-biventricular pacing (727 +/- 242 U) than during RA pacing (833 +/- 332 U) (p0.02). Furthermore, there was a positive correlation between baseline QRS duration and the decrease in SNA noted with RA-biventricular pacing (r = 0.58, p = 0.03). Biventricular pacing results in improved hemodynamics and a decrease in SNA compared with intrinsic conduction in patients with left ventricular dysfunction and IVCD. If the current findings are also present with chronic biventricular pacing, then this form of therapy may have a positive impact on mortality.

OBJECTIVESThe aim of this study was to determine the changes in sympathetic nerve activity (SNA) after atrioventricular junction (AVJ) ablation in patients with chronic atrial fibrillation (AF).BACKGROUNDPolymorphic ventricular tachycardia (PMVT) has been reported after AVJ ablation in patients paced at a rate of ≤70 beats/min. We hypothesized that AVJ ablation results in sympathetic neural changes that favor the occurrence of PMVT and that pacing at 90 beats/min attenuates these changes.METHODSSympathetic nerve activity, 90% monophasic cardiac action potential duration (APD90), right ventricular effective refractory period (ERP) and blood pressure measurements were obtained in 10 patients undergoing AVJ ablation. Sympathetic nerve activity was analyzed at baseline and during and after successful AVJ ablation for at least 10 min. Data were also collected after ablation at pacing rates of 60 and 90 beats/min. The APD90 and ERP were measured before and after AV block during pacing at 120 beats/min.RESULTSSympathetic nerve activity increased to 134 ± 16% of the pre-ablation baseline value (p < 0.01) after successful AVJ ablation plus pacing at 60 beats/min and decreased to 74 ± 8% of baseline (p < 0.05) with subsequent pacing at 90 beats/min. Both APD90 and ERP increased significantly.CONCLUSIONS1) Ablation of the AVJ followed by pacing at 60 beats/min is associated with an increase in SNA. 2) Pacing at 90 beats/min decreases SNA to or below the pre-ablation baseline value. 3) Cardiac APD and ERP increase after AVJ ablation. The increase in SNA, along with the prolongation in APD, may play a role in the pathogenesis of ventricular arrhythmias that occur after AVJ ablation.

Atrial stunning, as assessed by left atrial appendage emptying and increased spontaneous echo contrast, is known to occur following direct-current cardioversion of atrial fibrillation (AF) and atrial flutter (AFl). Little is known on atrial mechanical function and the time course of atrial recovery following radiofrequency ablation of AFl. Fourteen patients undergoing radiofrequency ablation of persistent typical counterclockwise AFl were enrolled. Two-dimensional and pulse Doppler transesophageal echocardiography (TEE) were performed before ablation and immediately following restoration of sinus rhythm. Left atrial spontaneous echo contrast grades, left atrial appendage emptying fractions, and peak left atrial appendage emptying velocities were measured. Transthoracic echocardiography (TTE) was performed immediately after ablation, then repeated after 1 day, 1 week, and 6 weeks to measure peak transmitral velocities and percent atrial contribution to ventricular filling. Left atrial appendage emptying velocities decreased significantly following AFl termination (44 ± 23 cm/s before ablation vs 25 ± 14 cm/s after ablation, p = 0.01). Left atrial appendage emptying fractions also decreased significantly (0.48 ± 0.1 preablation vs 0.34 ± 0.17 postablation, p = 0.02). New spontaneous echo contrast developed in 4 patients (29%) after ablation. Four patients had complete atrial standstill after ablation, and 1 patient developed a new left atrial appendage thrombus. The percent atrial contribution to ventricular filling recovered progressively over 6 weeks with significant improvement in peak transmitral velocities at day 7. Thus, atrial stunning occurs after catheter ablation of AFl and may lead to rapid formation of thrombus in the left atrial appendage. Significant improvement in left atrial function occurs in 7 days.

D the frequent use of amiodarone, questions about the effect of this drug on the defibrillation threshold (DFT) have not been fully answered. Previous clinical investigations have shown this drug to increase the DFT when using monophasic shocks,1–3 whereas other studies showed no effect.4 Implantable cardioverter-defibrillators (ICDs) now use biphasic waveforms because they are more effective in terminating ventricular fibrillation. Several recent uncontrolled studies comparing biphasic DFTs in populations of patients on and off amiodarone suggested no difference in the DFT between the 2 groups.5,6 Pelosi et al7 recently reported an increase in the biphasic DFT with chronic amiodarone use, measured on average 2 to 3 months after drug initiation, but provided no data regarding acute effects of the drug. We examined the immediate effects of in-hospital oral amiodarone loading on the biphasic DFT. • • • This study compared the DFTs of 18 patients (16 men and 2 women, mean age 63 6 10 years) at the time of initial implantation and after receiving an in-hospital load of oral amiodarone for clinically indicated reasons. The initial indication for ICD implantation was ventricular tachycardia in 17 patients and resuscitated cardiac death in 1 patient. Ten patients had underlying coronary artery disease, and 8 had dilated cardiomyopathy. Left ventricular function was severely depressed (,30%) in 15 patients; in 3 other patients it was moderately depressed (30% to 39%), mildly depressed (40% to 49%), and preserved (.50%). The implanted ICD models included the 7223Cx (n 5 7) and 7227Cx (n 5 6) manufactured by Medtronic, Inc. (Minneapolis, Minnesota), and the 1763 (n 5 1), 1782 (n 5 2), 1790 (n 5 1), and 1831 (n 5 1) manufactured by Guidant Corp. (St. Paul, Minnesota). All patients had DFTs determined at the time of device implant using a sequential “change in delivered energy” protocol from an initial delivered energy of 15 J with decrements or increments of 5 J. Ventricular fibrillation was induced using a T-wave shock. The lowest energy required for cardioversion was considered the DFT.8 No patient was receiving antiarrhythmic drugs other than b blockers (10 patients) at the time of initial device implant. The indication for amiodarone was recurrent ventricular tachycardia in 12 patients and atrial fibrillation in 6. The drug was loaded orally in the hospital for a total dose of 8 to 12 g over 6 to 10 days, followed by maintenance doses. Follow-up DFT determination was performed after the oral load using the same protocol used at device implant. The Student’s t test for paired data was used to compare the DFTs from implant and after amiodarone loading. Data are expressed as mean 6 SD. A p value ,0.05 was considered statistically significant. The time between initial DFT determination and the DFT after amiodarone loading ranged from 1 to 32 months. The average time between studies was 226 6 248 days, with a median time of 146 days. In the overall group, the DFT increased significantly after amiodarone loading, from 10.5 6 4.7 to 15.2 6 7.8 J (p ,0.0015). In the subgroup of patients in whom the time between initial DFT determination and initiation of amiodarone was ,6 months (12 of the 18 patients), the DFT also increased from 10.8 6 5.3 to 16.1 6 8.6 J (p 5 0.005). The mean changes in DFT are shown in Figure 1. After loading, 11 of 18 patients had an increase in the DFT, 6 had no change, and 1 patient had a decrease from 10 to 5 J. In 1 patient, termination of amiodarone was required because the DFT after drug loading was unacceptably high (25 J). Individual changes in the DFT are displayed in Figure 2. • • • The main finding of our study was the demonstration of higher DFTs using biphasic energy waveforms after in-hospital oral amiodarone loading over several days. To our knowledge, this is the first time that the effect of short-term amiodarone oral loading on the biphasic DFT has been examined in humans. Although the results observed in our study could be attributed to other long-term physiologic differences (such as changes in ventricular size and ventricular function), we doubt this to be the case. Three of 6 patients who began therapy with amiodarone within 1 month of the initial device implantation had an increase in the DFT after drug loading, including 1 patient whose DFT was raised enough to render an inadequate safety margin. The difference in DFT was also significant in the group of patients in whom amiodarone was started within 6 months of implant. Although the increase in defibrillation energy requirements was statistically significant, it was not universal. One third of patients studied had no change in the DFT after drug initiation, and 1 patient had a From the Department of Internal Medicine (Cardiology, Clinical Cardiac Electrophysiology), The University of Texas Southwestern Medical Center; and The Dallas Veterans Affairs Medical Center, Dallas, Texas. Dr. Joglar’s address is: Division of Cardiology, Department of Internal Medicine, University of Texas Southwestern Medical Center, Room CS7.102, 5323 Harry Hines Boulevard, Dallas, Texas 753909047. E-mail: jajogl@parknet.pmh.org. Manuscript received September 14, 2000; revised manuscript received and accepted March 27, 2001.

We conducted a prospective randomized study to determine the safety and efficacy rate of 3 commonly used energy levels (100, 200, and 360 J) for elective direct-current cardioversion of persistent atrial fibrillation. When compared with 100 and 200 J, the initial success rate with 360 J was significantly higher (14%, 39%, and 95%, respectively), and patients randomized to 360 J ultimately required less total energy and a lower number of shocks.

Scatterplots (displays of each RR interval as a function of the preceding RR interval) provide a visual assessment of nonrandom variations in heart rate. In a recent study, scatterplot length, width, and area correlated with time-domain measures of heart rate variability (HRV) in survivors of recent myocardial infarction (MI) receiving a beta blocker. We performed this study to (1) assess the relation between time-domain measures of HRV and scatterplot indexes in survivors of remote MI not receiving metoprolol and (2) to determine if metoprolol influenced scatterplot indexes. In 28 survivors of remote MI, HRV time-domain variables and scatterplot indexes were measured after 2 weeks off and 2 weeks on metoprolol. Off metoprolol, scatterplot length correlated with long-term HRV variables (SD of the difference of all RR intervals [r = 0.98], SD of the average of all 5-minute intervals [r = 0.97]), and scatterplot width correlated with short-term HRV variables (root-mean-square successive differences between RR intrevals [rMSSD] [r = 0.88]). Metoprolol increased time-domain HRV variables (mean RR interval, rMSSD, and proportion of adjacent RR intervals differing by > 50 ms [pNN50 (%)]) but did not alter scatterplot indexes. Thus, scatterplot indexes correlate with time-domain measures of HRV in survivors of remote MI not receiving metoprolol. In contrast to HRV time-domain variables, scatterplot indexes are not influenced by metoprolol.

In a series of 14 patients undergoing transseptal catheterization for ablation of left-sided accessory pathways, hydrogen appearance time was used to detect left-to-right shunting after removal of the catheter. Six of the 12 patients who had no evidence of shunt before catheterization had evidence of shunting after the procedure.

The use of non-thoracotomy endocardial implantable defibrillators with pacing capabilities has increased substantially over the past 2 years. This report demonstrates that the pacing threshold increases in some patients after endocardial defibrillation, and substantiates the practice of using maximal pacing output after endocardial defibrillation.