Acute Effects of Coffee Consumption on Health among Ambulatory Adults.

BACKGROUND: Coffee is one of the most commonly consumed beverages in the world, but the acute health effects of coffee consumption remain uncertain. METHODS: We conducted a prospective, randomized, case-crossover trial to examine the effects of caffeinated coffee on cardiac ectopy and arrhythmias, daily step counts, sleep minutes, and serum glucose levels. A total of 100 adults were fitted with a continuously recording electrocardiogram device, a wrist-worn accelerometer, and a continuous glucose monitor. Participants downloaded a smartphone application to collect geolocation data. We used daily text messages, sent over a period of 14 days, to randomly instruct participants to consume caffeinated coffee or avoid caffeine. The primary outcome was the mean number of daily premature atrial contractions. Adherence to the randomization assignment was assessed with the use of real-time indicators recorded by the participants, daily surveys, reimbursements for date-stamped receipts for coffee purchases, and virtual monitoring (geofencing) of coffee-shop visits. RESULTS: The mean (±SD) age of the participants was 39±13 years; 51% were women, and 51% were non-Hispanic White. Adherence to the random assignments was assessed to be high. The consumption of caffeinated coffee was associated with 58 daily premature atrial contractions as compared with 53 daily events on days when caffeine was avoided (rate ratio, 1.09; 95% confidence interval [CI], 0.98 to 1.20; P = 0.10). The consumption of caffeinated coffee as compared with no caffeine consumption was associated with 154 and 102 daily premature ventricular contractions, respectively (rate ratio, 1.51; 95% CI, 1.18 to 1.94); 10,646 and 9665 daily steps (mean difference, 1058; 95% CI, 441 to 1675); 397 and 432 minutes of nightly sleep (mean difference, 36; 95% CI, 25 to 47); and serum glucose levels of 95 mg per deciliter and 96 mg per deciliter (mean difference, -0.41; 95% CI, -5.42 to 4.60). CONCLUSIONS: In this randomized trial, the consumption of caffeinated coffee did not result in significantly more daily premature atrial contractions than the avoidance of caffeine. (Funded by the University of California, San Francisco, and the National Institutes of Health; CRAVE ClinicalTrials.gov number, NCT03671759.).

Increased heart rate due to supra-ventricular tachycardia triggering premature ventricular contraction.

We describe a case wherein the presence of premature ventricular contractions was related to an increased heart rate that occurred due to supra-ventricular tachycardia: atrial tachycardia or atrioventricular nodal reentry tachycardia.

Noninvasive light emitting diode therapy: A novel approach for postinfarction ventricular arrhythmias and neuroimmune modulation.

BACKGROUND: Sympathetic neural activation plays a key role in the incidence and maintenance of acute myocardial infarction (AMI) induced ventricular arrhythmia (VA). Furthermore, previous studies showed that AMI might induce microglia and sympathetic activation and that microglial activation might contribute to sympathetic activation. Recently, studies showed that light emitting diode (LED) therapy might attenuate microglial activation. Therefore, we hypothesized that LED therapy might reduce AMI-induced VA by attenuating microglia and sympathetic activation. METHODS: Thirty anesthetized rats were randomly divided into three groups: the Control group (n = 6), AMI group (n = 12), and AMI + LED group (n = 12). Electrocardiogram (ECG) and left stellate ganglion (LSG) neural activity were continuously recorded. The incidence of VAs was recorded during the first hour after AMI. Furthermore, we sampled the brain and myocardium tissue of the different groups to examine the microglial activation and expression of nerve growth factor (NGF), interleukin-18 (IL-18), and IL-1ß, respectively. RESULTS: Compared to the AMI group, LED therapy significantly reduced the incidence of AMI-induced VAs (ventricular premature beats [VPB] number: 85.08 ± 13.91 vs 27.5 ± 9.168, P < .01; nonsustained ventricular tachycardia (nSVT) duration: 34.39 ± 8.562 vs 9.005 ± 3.442, P < .05; nSVT number: 18.92 ± 4.52 vs 7.583 ± 3.019, P < .05; incidence rate of SVT/VF: 58.33% vs. 8.33%, P < .05) and reduced the LSG neural activity (P < .01) in the AMI + LED group. Furthermore, LED significantly attenuated microglial activation and reduced IL-18, IL-1ß, and NGF expression in the peri-infarct myocardium. CONCLUSION: LED therapy may protect against AMI-induced VAs by suppressing sympathetic neural activity and the inflammatory response.

2019 HRS/EHRA/APHRS/LAHRS expert consensus statement on catheter ablation of ventricular arrhythmias.

Ventricular arrhythmias are an important cause of morbidity and mortality and come in a variety of forms, from single premature ventricular complexes to sustained ventricular tachycardia and fibrillation. Rapid developments have taken place over the past decade in our understanding of these arrhythmias and in our ability to diagnose and treat them. The field of catheter ablation has progressed with the development of new methods and tools, and with the publication of large clinical trials. Therefore, global cardiac electrophysiology professional societies undertook to outline recommendations and best practices for these procedures in a document that will update and replace the 2009 EHRA/HRS Expert Consensus on Catheter Ablation of Ventricular Arrhythmias. An expert writing group, after reviewing and discussing the literature, including a systematic review and meta-analysis published in conjunction with this document, and drawing on their own experience, drafted and voted on recommendations and summarized current knowledge and practice in the field. Each recommendation is presented in knowledge byte format and is accompanied by supportive text and references. Further sections provide a practical synopsis of the various techniques and of the specific ventricular arrhythmia sites and substrates encountered in the electrophysiology lab. The purpose of this document is to help electrophysiologists around the world to appropriately select patients for catheter ablation, to perform procedures in a safe and efficacious manner, and to provide follow-up and adjunctive care in order to obtain the best possible outcomes for patients with ventricular arrhythmias.

Prediction of premature ventricular complex origin in left vs. right ventricular outflow tract: a novel anatomical imaging approach.

AIMS: Left ventricular (LV) outflow tract ventricular arrhythmias (OTVA) are associated with hypertension (HT), older age, and LV dysfunction, suggesting that LV overload plays a role in the aetiopathogenesis. We hypothesized that anatomical modifications of the LV outflow tract (LVOT) could predict left vs. right OTVA site of origin (SOO). METHODS AND RESULTS: Fifty-six (32 men, 53 ± 18 years old) consecutive patients referred for OTVA ablation were included. Cardiac multidetector computed tomography was performed before ablation and then imported to the CARTO system to aid the mapping and ablation procedure. Anatomical characteristics of the aortic root as well as aortopulmonary valvular planar angulation (APVPA) were analysed. The LV was the OTVA SOO (LVOT-VA) in 32 (57%) patients. These patients were more frequently male (78% vs. 22%, P = 0.001), older (57 ± 18 vs. 47 ± 18 years, P = 0.055), and more likely to have HT (59% vs. 21%, P = 0.004), compared to right OTVA patients. Aortopulmonary valvular planar angulation was higher in LVOT-VA patients (68 ± 5° vs. 55 ± 6°, respectively; P < 0.001). Absolute size of all aortic root diameters was associated with LVOT origin. However, after indexing by body surface area, only sinotubular junction diameter maintained a significant association (P = 0.049). Multivariable analysis showed that APVPA was an independent predictor of LVOT origin. Aortopulmonary valvular planar angulation ≥62° reached 94% sensitivity and 83% specificity (area under the curve 0.95) for predicting LVOT origin. CONCLUSIONS: The measurement of APVPA as a marker of chronic LV overload is useful for the prediction of left vs. right ventricular OTVA origin.

Chronic median nerve modulation reduces ventricular arrhythmia and improves ventricular function in a postmyocardial infarction rabbit model.

AIM: Median nerve stimulation (MNS) is a novel neuromodulation approach for treatment of ventricular arrhythmia, but little is known about its chronic effects. The aim of this study was to investigate the effects of chronic MNS on ventricular arrhythmia and ventricular dysfunction postmyocardial infarction (MI). METHOD: Two weeks after MI, 12 rabbits were randomly divided into control and MNS groups, and chronic MNS was performed in MNS group for 2 weeks. Ventricular function and arrhythmias; sympathetic innervation and activity; and interleukin-1 ß (IL-1 ß) and norepinephrine (NE) levels were analyzed. RESULTS: Both the total number of premature ventricular complex and episodes of ventricular tachycardia were lower in MNS group than in control group (20 560 ± 10 314 beats vs 70 079 ± 37 184 beats, P = .021, and 115 ± 63 episodes vs 307 ± 164 episodes, P = .034, respectively). Compared with control group, MNS decreased the cardiac sympathetic nerve density and level of circulating NE in MNS group (1798.42 ± 644.07 µm2 /mm2 vs 1003.79 ± 453.00 µm2 /mm2, P = .041, and 20.86 ± 4.54 pg/mL vs 11.07 ± 1.43 pg/mL, P = .002, respectively). MNS also improved the left ventricular ejection fraction (59.07 ± 1.91% vs 49.77 ± 3.47%, P = .003) and inhibited the level of IL-1 ß in serum (69.19 ± 4.71 pg/mL vs 85.93 ± 12.80 pg/mL, P = .013). CONCLUSION: Chronic MNS appears to protect against ventricular arrhythmia and improves ventricular function post-MI, which may be mediated by suppressing cardiac sympathetic activity and anti-inflammatory effects.

Proof of concept study of a novel pacemapping algorithm as a basis to guide ablation of ventricular arrhythmias.

Aims: To determine if a software algorithm can use an individualized distance-morphology difference model, built from three initial pacemaps, to prospectively locate the exit site (ES) of ventricular arrhythmias (VA). Methods and results: Consecutive patients undergoing ablation of VA from a single centre were recruited. During mapping, three initial pacing points were collected in the chamber of interest and the navigation algorithm applied to predict the ES, which was corroborated by conventional mapping techniques. Thirty-two patients underwent ES prediction over 35 procedures. Structural heart disease was present in 16 (7 ischaemic cardiomyopathy, 9 non-ischaemic cardiomyopathy), median ejection fraction 45% [Interquartile range (IQR) 26]. The remainder had normal hearts. The navigation algorithm was applied to 46 VA (24 left ventricle, 11 right ventricular outflow tract, 5 left ventricular outflow tract, 4 right ventricle, 2 epicardial) and successfully located the site of best pacemap match in 45 within a median area of 196.5 mm2 (IQR 161.3, range 46.6-1288.2 mm2). Conclusions: In a diverse population of patients with and without structural heart disease, the ES of VA can be accurately and reliably identified to within a clinically useful target area using a simple software navigation algorithm based on pacemapping.

Feasibility of Performing Radiofrequency Catheter Ablation and Endomyocardial Biopsy in the Same Setting.

In patients with unexplained cardiomyopathy, electroanatomical mapping can identify abnormal tissue to target during electrophysiology-guided endomyocardial biopsy (EP-guided EMB). The objective of this study is to determine whether catheter ablation performed in the same setting as EP-guided EMB increases procedural risk. Sixty-seven patients (mean age 54.4 ± 13.8, 57% male) undergoing EP-guided EMB were included. Radiofrequency catheter ablation was performed in 17 patients (25%) for ventricular arrhythmias and in 2 (3%) for typical atrial flutter. Femoral arterial access was obtained in 90% ablation patients and 40% biopsy-only patients; vascular access complications were more common in the ablation group than in the EMB-only group (p = 0.02). There were no significant differences in rate of tricuspid regurgitation, thromboembolism, or pericardial effusion, whether procedural anticoagulation was used. In conclusion, catheter ablation and procedural anticoagulation can be combined with EP-guided EMB with an increased risk of vascular access complications, but no significant increase in intracardiac complications.

Wenxin Keli for Ventricular premature complexes with Heart failure: A Systematic Review and Meta-Analysis of Randomized Clinical Trials.

OBJECTIVE: To evaluate the efficacy and safety of Wenxin Keli (WXKL) alone or combined with Western medicine in treating ventricular premature complexes (VPCs) with heart failure (HF). METHODS: We searched five databases to identify relevant randomized controlled trials (RCTs) published before May 2016. Two review authors independently searched and screened the literature, extracted the data as well as assessed the methodological quality of the included studies by using criteria from the Cochrane Handbook, and analyzed via using Review Manager 5.3 software. RESULTS: Eight studies of WXKL were included. The results of the Meta-analysis showed that WXKL was more significant on the frequency of VPCs (MD=-427.08, 95% CI: -526.73∼-327.43, P<0.01), left ventricular ejection fraction (LVEF) (MD=-4.12, 95% CI: 2.97∼5.27, P<0.01), the total effect of VPCs (RR=0.48, 95% CI: 0.34∼0.69, P<0.01) and 6-min walking test (MD=28.05, 95% CI: 19.56∼36.54, P<0.01). The treatment group presented a significant reduction at left ventricular end-diastolic diameter (LVED) (MD=-3.94, 95% CI: -6.57∼-1.31, P<0.01) when treatment time was 12 weeks, however, there was no statistical difference at 8 weeks. In addition, the included trials generally showed low methodological quality. CONCLUSIONS: Wenxin Keli may be effective and safe for treating VPCs and HF. However, further RCTs of larger scale, multi-center/country, longer follow-up periods, and higher quality are still required to verify the efficacy of Wenxin Keli in ventricular premature beat with heart failure.

Idiopathic ventricular arrhythmias: Relevance to the anatomy, diagnosis and treatment.

Idiopathic ventricular arrhythmias (VAs) are ventricular tachycardias (VTs) or premature ventricular contractions (PVCs) whose mechanisms are not related to myocardial scar. Idiopathic VAs occur most commonly without structural heart disease, but can occur with structural heart disease. Imaging tests, such as echocardiography, nuclear test, and cardiac magnetic resonance imaging, are helpful for excluding any association of an idiopathic VA occurrence with myocardial scar. Since catheter ablation emerged, the sites of idiopathic VA origins, commonly endocardial but sometimes epicardial, have been increasingly recognized. Idiopathic VAs usually originate from specific anatomical structures, and exhibit characteristic electrocardiograms based on their anatomical background. Idiopathic VAs are basically benign, but they require medical treatment or catheter ablation when idiopathic VAs are symptomatic, incessant, or produce left ventricular dysfunction. This review describes the up-to-date information on the prevalence of idiopathic VA origins relevant to the anatomy, and diagnosis, and treatment of idiopathic VAs.

Ventricular tachycardia originating from the septal papillary muscle of the right ventricle: electrocardiographic and electrophysiological characteristics.

INTRODUCTION: Premature ventricular complexes (PVCs) and ventricular tachycardia (VT) arising from papillary muscles of both ventricles have recently been described. There is a lack of data on VT originating from the right ventricular papillary (RV PAP) muscles. There have been no prior studies focused on the electrocardiogram (ECG) features and ablation of PVC/VT arising from the septal papillary muscle of the right ventricle. METHODS: Among 155 consecutive patients with normal structural heart who underwent catheter ablation of PVC/VT, 8 patients with PVC/VT from the septal RV PAP muscle were identified. The site of origin of the arrhythmias was identified through activation/pace mapping and intracardiac echocardiography. All patients underwent radiofrequency ablation of the arrhythmia. RESULTS: Data on 8 consecutive patients (2 men, age 42 ± 13 years old) were collected. All patients had a preserved ejection fraction (60 ± 4%). Septal RV PAP arrhythmias had a left superior axis and negative concordance or late R-wave transition in precordial leads. PVCs were spontaneous in 5 cases, were induced by isoprotenerol in 2 cases and by isoproterenol plus phenylephrine in another one. PVCs were never induced with calcium bolus and only rarely with burst pacing. Adenosine never terminated VT or suppressed the VT/PVCs. Radiofrequency, fluoroscopic, and procedural time were, respectively, 10.3 ± 3, 36.4 ±11.3, and 76.3 ± 27.5 minutes. During a mean follow-up of 8 ± 4 months, mean PVC burden was reduced from 14 ± 3% preablation to 0.1 ± 0.2% postablation. CONCLUSION: PVCs and VT originating from septal RV papillary muscle could have a typical ECG pattern due to the site of the muscle involved. Radiofrequency ablation of this anatomic area is feasible and effective.

Electrophysiologic characteristics of ventricular arrhythmias arising from the aortic mitral continuity-potential role of the conduction system.

INTRODUCTION: Catheter ablation of ventricular arrhythmia (VA) at the fibrous aortic mitral continuity (AMC) has been described, yet the nature of the arrhythmogenic substrate remains unknown. METHODS: Procedural records of 528 consecutive patients undergoing ablation of VA at Mayo Clinic, Rochester, MN, were reviewed. The electrocardiographic and electrophysiologic characteristics of patients with successful ablation at the AMC were analyzed to characterize the underlying arrhythmogenic substrate. RESULTS: Of the 21 patients (mean age 53.2 ± 13.4 years, 47.6% male) who underwent ablation of VA at the AMC with acute success, prepotentials (PPs) were found at the ablation sites preceding the ventricular electrogram (VEGM) during arrhythmias in 13 (61.9%) patients and during sinus rhythm in 7 (53.8%) patients. VAs with PPs were associated with a significantly higher burden of premature ventricular complexes (PVCs; 26.1 ± 10.9% vs. 14.9 ± 10.1%, P = 0.03), shorter VEGM to QRS intervals (9.0 ± 28.5 milliseconds vs. 33.1 ± 8.8 milliseconds, P = 0.03), lower pace map scores (8.7 ± 1.6 vs. 11.4 ± 0.8, P = 0.001), and a trend toward shorter V-H intervals during VA (32.1 ± 38.6 milliseconds vs. 76.3 ± 11.1 milliseconds, P = 0.06) as compared to those without PP. A strong and positive correlation was found between V-H interval and QRS duration during arrhythmia in those with PPs (B = 2.11, R(2) = 0.97, t = 13.7, P < 0.001) but not in those without PPs. CONCLUSION: Local EGM characteristics and relative activation time of the His bundle suggest the possibility of conduction tissue as the origin for VA arising from the fibrous AMC. Specific identification and targeting of PPs when ablating VAs at this location may improve procedural success.

Ablation of ventricular arrhythmias.

Ventricular arrhythmias (VAs) commonly occur in patients with structural heart disease and may present as ventricular premature depolarizations (VPDs), monomorphic ventricular tachycardia (VT), or polymorphic VT/ventricular fibrillation. Idiopathic VAs can also occur in patients with normal hearts. This review explores the etiology, clinical presentation, and management strategies for different types of VAs. Medical and invasive treatment strategies are discussed, and different approaches to catheter ablation are outlined. While ablation of VPDs and idiopathic VT provides a cure for the majority of patients, investigation is ongoing to define the optimal ablation strategy for patients with scar-related VT.

Carotid baroreceptor stimulation prevents arrhythmias induced by acute myocardial infarction through autonomic modulation.

: Electrical carotid baroreceptor stimulation (CBS) has shown therapeutic potential for resistant hypertension and heart failure by resetting autonomic nervous system, but the impacts on arrhythmias remains unclear. This study evaluated the effects of CBS on ventricular electrophysiological properties in normal dog heart and arrhythmias after acute myocardial infarction (AMI). In the acute protocol, anesthetized open chest dogs were exposed to 1 hour left anterior descending coronary occlusion as AMI model. Dogs were received either sham treatment (Control group, n = 8) or CBS (CBS group, n = 8), started 1 hour before AMI. CBS resulted in pronounced prolongation of ventricular effective refractory period and reduction of the maximum action potential duration restitution slope (from 0.85 ± 0.15 in the baseline state to 0.67 ± 0.09 at the end of 1 hour, P < 0.05) before AMI. Number of premature ventricular contractions (277 ± 168 in the Control group vs. 103 ± 84 in the CBS group, P < 0.05) and episodes of ventricular tachycardia/ventricular fibrillation (7 ± 3 in the Control group vs. 3 ± 2 in the CBS group, P < 0.05) was decreased compared with the control group during AMI. CBS buffered low-frequency/high-frequency ratio raise during AMI. Ischemic size was not affected by CBS. CBS may have a beneficial impact on ventricular arrhythmias induced by AMI through modulation of autonomic tone.

Ubiquitous myocardial extensions into the pulmonary artery demonstrated by integrated intracardiac echocardiography and electroanatomic mapping: changing the paradigm of idiopathic right ventricular outflow tract arrhythmias.

BACKGROUND: Idiopathic ventricular arrhythmias of left bundle branch block inferior axis morphology are usually localized to the right ventricular outflow tract (RVOT), presumably below the pulmonic valve (PV). However, the PV location is usually not confirmed by direct visualization. METHODS AND RESULTS: Intracardiac echocardiography was used to visualize and tag the PV annulus, which was then integrated with 3-dimensional voltage maps of the RVOT. Distances were measured from the furthest extent of myocardial signal (bipolar voltage ≥1.5 mV) to the PV annulus. This was performed in 24 control patients and 24 prospective patients with RVOT arrhythmias. Myocardial signal beyond the PV was found in 92% of controls and 88% of RVOT arrhythmia patients (P=1.000). Average myocardial extension was further on the septal side than on the free wall side for control patients (5.6 mm; interquartile range [IQR], 3.6-7.7, versus 1.7 mm; IQR (-)0.1 to (+)4.0; P=0.002) and RVOT arrhythmia patients (5.7 mm; IQR, 2.7-7.7, versus 1.4 mm; IQR, (-)0.8 to (+)4.8; P=0.004). Eleven (46%) RVOT arrhythmia foci were localized beyond the valve in the pulmonary artery (median 8.2 mm above PV; IQR, 6.6-10.3 mm); these locations were confirmed as supravalvular by direct intracardiac echocardiography visualization. CONCLUSIONS: Myocardial voltage extension into the pulmonary artery in humans is ubiquitous and can be demonstrated in vivo using 3-dimensional integrated intracardiac echocardiography to localize the PV. These extensions frequently serve as origins of presumed RVOT arrhythmias; intracardiac echocardiography localization of the PV allows reclassification of these as pulmonary arterial arrhythmias.

The Brockenbrough-Braunwald-Morrow sign.

Hypertrophic cardiomyopathy is a relatively common genetic disorder and usually asymptomatic. However, approximately 25% of patients develop left ventricular outflow obstruction and can develop angina, syncope, or congestive heart failure. Initiation and titration of beta-blockade usually results in symptomatic improvement. Patients with medically refractory symptoms can see further symptomatic improvement and relief of obstruction with either surgical myectomy or alcohol septal ablation (ASA). Although surgical myectomy has been the gold standard, ASA has been shown in nonrandomized studies and a meta-analysis to be comparable. In patients undergoing ASA without a rest obstruction, the Brokenbrough-Braunwald-Morrow sign can be used to accurately determine the degree of left ventricular outflow tract (LVOT) obstruction prior to, during, and after ASA.

Induced and spontaneous heart rate turbulence in mice: influence of coupling interval.

AIMS: Heart rate turbulence (HRT) is a prognostic parameter for risk stratification in patients suffering from coronary artery disease. The aims of this study were to demonstrate the feasibility of quantifying HRT in mice, both in long-term electrocardiograms (ECGs) as well as after extrastimulus pacing, and to analyse its characteristics. METHODS AND RESULTS: We performed long-term ECG recordings using implanted telemetric chips and electrophysiological (EP) investigations, using transvenously inserted EP catheters, in healthy mice. Heart rate turbulence was calculated using the established turbulence onset (TO) and slope (TS) algorithm. After spontaneous ventricular premature complexes (VPCs), we found a negative TO (-2.2 ± 7.5%) and positive TS (15.5 ± 18.3 ms/RR interval). Electrophysiological investigations revealed positive values for TO (0.6 ± 1.1%) and TS (6.5 ± 2.9 ms/RR interval) after extrastimulus pacing maneuvers. The shortening of the extrastimuli coupling intervals delivered during EP investigations significantly influenced TO (r = 0.57; P = 0.01): shorter coupling intervals provoked more positive TO values. CONCLUSION: Mice display both spontaneous and induced HRT. In terms of TO, VPCs generated by extrastimulus pacing are significantly dependent on the coupling interval. Determining HRT in mice is feasible and provides insight into basic mechanisms of blood pressure regulation, which is realized by the baroreflex.