Right ventricular dysfunction as an echocardiographic prognostic factor in hemodynamically stable patients with acute pulmonary embolism: a meta-analysis.

BACKGROUND: We investigated whether right ventricular dysfunction (RVD) as assessed by echocardiogram can be used as a prognostic factor in hemodynamically stable patients with acute pulmonary embolism (PE). Short-term mortality has been investigated only in small studies and the results have been controversial. METHODS: A PubMed search was conducted using two keywords, "pulmonary embolism" and "echocardiogram", for articles published between January 1st 1998 and December 31st 2011. Out of 991 articles, after careful review, we found 12 articles that investigated the implications of RVD as assessed by echocardiogram in predicting short-term mortality for hemodynamically stable patients with acute PE. We conducted a meta-analysis of these data to identify whether the presence of RVD increased short-term mortality. RESULTS: Among 3283 hemodynamically stable patients with acute PE, 1223 patients (37.3%) had RVD, as assessed by echocardiogram, while 2060 patients (62.7%) had normal right ventricular function. Short-term mortality was reported in 167 (13.7%) out of 1223 patients with RVD and in 134 (6.5%) out of 2060 patients without RVD. Hemodynamically stable patients with acute PE who had RVD as assessed by echocardiogram had a 2.29-fold increase in short-term mortality (odds ratio 2.29, 95% confidence interval 1.61-3.26) compared with patients without RVD. CONCLUSIONS: In hemodynamically stable patients with acute PE, RVD as assessed by echocardiogram increases short-term mortality by 2.29 times. Consideration should be given to obtaining echocardiogram to identify high-risk patients even if they are hemodynamically stable.

Submaximal cardiopulmonary exercise testing for the evaluation of unexplained dyspnea.

OBJECTIVES: Gas exchange measurements obtained during submaximal exercise have been shown to provide prognostic and diagnostic information in patients with heart failure (HF) and to differentiate heart versus lung limitations in patients with unexplained dyspnea. The aim of our study was to assess the clinical utility of submaximal cardiopulmonary exercise testing using the Shape-HF equipment in identifying the cause of unexplained dyspnea. METHODS: A total of 65 patients underwent Shape-HF tests from September 2010 to June 2011 for unexplained dyspnea at our center. RESULTS: Of 65 patients, 39 were men and 26 were women. In this study, 23 patients had preexisting asthma or chronic obstructive pulmonary disease (COPD); 19 patients had a pacemaker (8), an implantable cardioverter defibrillator (2), or a cardiac resynchronization therapy defibrillator (CRT-D) (9). The study revealed that submaximal cardiopulmonary exercise testing provided supportive clinical data for deconditioning, pulmonary limitations (eg, COPD, interstitial lung disease, sleep apnea), pulmonary hypertension, and chronotropic incompetence in 21.5%, 23.1%, 13.8%, and 6.2% of patients, respectively. Pulmonary hypertension was confirmed in 55% of patients by echocardiography and lung problems were confirmed in 40% of patients by pulmonary function test and sleep study. Of nine patients with an implanted CRT-D, optimization of atrioventricular and interventricular programming was performed in seven (78%) using gas exchange monitoring while performing a steady state, low-level treadmill walk. CONCLUSIONS: Submaximal cardiopulmonary exercise testing has strongly suggested the diagnosis of COPD, interstitial lung disease, pulmonary hypertension, and deconditioning and has led to appropriate testing. Based on prior studies, we also used Shape-HF for its approved purpose of optimizing CRT-D programming in patients with HF, leading to clinical improvement.

Design and Validation of a Soft Robotic Simulator for Transseptal Puncture Training.

OBJECTIVE: Transseptal puncture (TP) is the technique used to access the left atrium of the heart from the right atrium during cardiac catheterization procedures. Through repetition, electrophysiologists and interventional cardiologists experienced in TP develop manual skills to navigate the transseptal catheter assembly to their target on the fossa ovalis (FO). Cardiology fellows and cardiologists that are new to TP currently train on patients to develop this skill, resulting in increased risk of complications. The goal of this work was to create low-risk training opportunities for new TP operators. METHODS: We developed a Soft Active Transseptal Puncture Simulator (SATPS), designed to match the dynamics, static response, and visualization of the heart during TP. The SATPS includes three subsystems: (i) A soft robotic right atrium with pneumatic actuators mimics the dynamics of a beating heart. (ii) A fossa ovalis insert simulates cardiac tissue properties. (iii) A simulated intracardiac echocardiography environment provides live visual feedback. Subsystem performance was verified with benchtop tests. Face and content validity were evaluated by experienced clinicians. RESULTS: Subsystems accurately represented atrial volume displacement, tenting and puncture force, and FO deformation. Passive and active actuation states were deemed suitable for simulating different cardiac conditions. Participants rated the SATPS as realistic and useful for training cardiology fellows in TP. CONCLUSION: The SATPS can help improve catheterization skills of novice TP operators. SIGNIFICANCE: The SATPS could provide novice TP operators the opportunity to improve their TP skills before operating on a patient for the first time, reducing the likelihood of complications.

Leadless Pacemaker Implantation in a Patient With Diminutive Subclavian Veins.

BACKGROUND: Conventional pacemakers have a longstanding history of preventing morbidity and mortality in patients with bradyarrhythmia and conduction disorders. While decades of advancements have improved pacemaker technology and implantation technique, insertion of transvenous leads and formation of a pectoral pocket can lead to complications, including pocket hematoma, pneumothorax, or infection. Leadless pacemakers were introduced in 2012 to address these complications; however, early leadless systems only provided single-chamber ventricular pacing. In 2020, an accelerometer-based atrial sensing feature was developed to allow for atrioventricular (AV) synchrony with these devices. Early evidence suggests that patients with sinus rhythm and AV block can benefit from single-chamber leadless pacing systems with an AV synchrony algorithm. As availability of these devices continues to broaden, identification of appropriate recipients has become increasingly relevant.

Multiple episodes of ventricular tachycardia induced by silent coronary vasospasm.

We present a 46-year-old patient who suffered from cardiac arrest and subsequently underwent placement of an implantable cardioverter defibrillator (ICD). The patient underwent a cardiac catheterization which revealed no significant coronary artery disease. About 1 year later he experienced appropriated and frequent ICD discharges due to monomorphic ventricular tachycardia (VT) with left bundle branch block morphology. His prodromal symptoms were mild dizziness and lightheadedness with no chest pain. Amiodarone, mexiletine, sotalol and dofetilide as well as ablation of two inducible ventricular tachycardias in the electrophysiology studies were unsuccessful in controlling the arrhythmias and ICD discharges. During the last episode, he experienced a mild burning sensation in his chest and was given nitroglycerin 0.4 mg sublingually, which relived his symptoms and aborted the VT. This led to a second cardiac catheterization to investigate whether the VT was being induced by myocardial ischemia. This second coronary angiogram spontaneously revealed significant coronary vasospasm and simultaneously, the patient's cardiac rhythm showed short runs of VT with left bundle branch block morphology. Intracoronary nitroglycerine relieved the coronary vasospasm and terminated the arrhythmia. The patient was treated with isosorbide mononitrate and diltiazem. He remained symptom free with no ICD discharges and no VT in ICD interrogations for more than 2 years. Coronary vasospasm may be silent and with no chest pain which creates a difficult clinical situation particularly if it is associated with ventricular tachycardia and sudden cardiac death. The mechanisms of VT in the setting of coronary vasospasm are not known and increased automaticity, focal discharges, functional unidirectional block with reentry, or a combination of these mechanisms may contribute to inducing the VT during the transient ischemia or rarely in the reperfusion phase. It is important to perform provocative tests to diagnose silent coronary vasospasm in unexplained sudden cardiac arrests.

Creation and Implementation of an Outpatient Pathway for Atrial Fibrillation in the Emergency Department Setting: Results of an Expert Panel.

Atrial fibrillation and flutter (AF) is a common condition among emergency department (ED) patients in the United States. Traditionally, ED care for primary complaints related to AF focus on rate control, and patients are often admitted to an inpatient setting for further care. Inpatient care may include further telemetry monitoring and diagnostic testing, rhythm control, a search for identification of AF etiology, and stroke prophylaxis. However, many patients are eligible for safe and effective outpatient management pathways. They are widely used in Canada and other countries but less widely adopted in the United States. In this project, we convened an expert panel to create a practical framework for the process of creating, implementing, and maintaining an outpatient AF pathway for emergency physicians to assess and treat AF patients, safely reduce hospitalization rates, ensure appropriate stroke prophylaxis, and effectively transition patients to longitudinal outpatient treatment settings from the ED and/or observation unit. To support local pathway creation, the panel also reached agreement on a protocol development plan, a sample pathway, consensus recommendations for pathway components, sample pathway metrics, and a structured literature review framework using a modified Delphi technique by a technical expert panel of emergency medicine, cardiology, and other stakeholder groups.

ST segment elevation on electrocardiogram: the electrocardiographic pattern of Brugada syndrome.

A 77-year-old white diabetic woman was brought to our emergency department (ED) after becoming lightheaded and hypotensive at home. Her routine tests including a chest radiograph were normal. Her electrocardiogram (ECG) showed significant ST segment elevation in leads V1 to V4. Serial cardiac enzymes and troponin were within normal limits. Her ECG met the criteria for type 1 Brugada syndrome. Brugada syndrome, which is more common in young Asian males, is an arrhythmogenic disease caused in part by mutations in the cardiac sodium channel gene SCN5A. To diagnose the Brugada syndrome, 1 ECG criterion and 1 clinical criterion should exist. Brugada syndrome can be associated with ventricular tachycardia or fibrillation; the only treatment proven to prevent sudden death is placement of an implantable cardioverter defibrillator, which is recommended in symptomatic patients or in those with ventricular tachycardia induced during electrophysiologic studies and a type 1 ECG pattern of Brugada syndrome. It is important to recognize the Brugada ECG pattern and to differentiate it from other etiologies of ST segment elevation on ECG.

Brugada syndrome unmasked by pneumonia.

A 69-year-old white woman presented at our emergency room with right-side pleuritic chest pain, fever, and tachycardia. Results of the physical examination, routine laboratory tests, and chest radiography were unexceptional. An electrocardiogram showed ST elevation in leads V(1) through V(3) with T-wave inversion. Because of the chest pain and the ST elevation, the patient underwent emergency cardiac catheterization, which showed no coronary artery stenosis. A computed tomographic scan of the chest showed pulmonary infiltration in the right middle lobe and the lingula of the left upper lobe; pneumonia was diagnosed, and appropriate antibiotic therapy was started. The electrocardiographic changes met the criteria for type-1 Brugada pattern. Brugada syndrome is an arrhythmogenic disease caused in part by mutations in the cardiac sodium channel gene SCN5A. When the sodium current is disrupted, the outward transient current at the end of phase 1 of the action potential becomes unopposed. This creates a voltage gradient between the epicardium and endocardium, especially in the right ventricular wall, which leads to J-point elevation in leads V(1) through V(3). Fever exaggerates this defect in sodium channels. In our patient, the pleuritic chest pain was caused by the pneumonia, and the ST elevation was probably related to Brugada syndrome, unmasked by the febrile episode. Brugada syndrome can be associated with ventricular tachycardia or fibrillation; the only treatment proven to prevent sudden death is placement of an implantable cardioverter defibrillator, which is recommended in symptomatic patients or in those with ventricular tachycardia induced during electrophysiologic studies.

Hybrid therapy with right atrial catheter ablation and previously ineffective antiarrhythmic drugs for the management of atrial fibrillation.

BACKGROUND: Many patients with paroxysmal atrial fibrillation (AF) become refractory to antiarrhythmic drugs (AADs). Early studies suggested that linear catheter ablation in the right atrium may provide sufficient substrate modification to reestablish therapeutic efficacy of previously ineffective AADs. METHODS: This prospective before-after multicenter trial evaluated the safety and effectiveness of hybrid therapy that included right atrial catheter ablation coupled with a regimen of previously ineffective AADs on AF episode frequency and symptoms in drug refractory patients with paroxysmal AF. A standard linear lesion set (lateral, septal, isthmus) was used in all subjects. AF episode frequency, clinical arrhythmia symptoms, condition-specific (AFSS) and global health-related quality of life (SF-36) were assessed prior to ablation and at 6 months. RESULTS: Ninety-three subjects, refractory to an average 2.9 AADs at baseline, qualified for inclusion and underwent right atrial catheter ablation. Eighty-four subjects (90%) provided 6 month AF episode frequency data which demonstrated a significant decrease compared to baseline (3.4 vs. 9.5, p < 0.0001). Forty-nine subjects (58%) were considered a clinical success by virtue of achieving a pre-specified target level episode frequency reduction of 50% or greater. Substantial and statistically significant improvements were realized almost uniformly for all measured arrhythmia symptoms as well as for both quality of life measures. The incidence of major complications was 5.4%. CONCLUSIONS: The addition of right atrial catheter ablation to a regimen of previously ineffective AADs is associated with a significant reduction in the frequency, duration and severity of AF episodes and symptoms.

Screening of young competitive athletes for the prevention of sudden cardiac death with a wireless electrocardiographic transmission device: a pilot study.

BACKGROUND: The 12-lead electrocardiographic screening for the prevention of sudden cardiac death in young competitive athletes is not cost-effective and thus not routinely recommended. We investigate whether a less expensive wireless electrocardiographic transmission device can be used to screen for the prevention of sudden cardiac death in this population. METHODS: During pre-participation screening, twenty college football players underwent two electrocardiograms: a conventional 12-lead electrocardiogram and a wireless 9-lead electrocardiogram. We compared several electrocardiographic parameters (QRS duration, left ventricular hypertrophy using the Cornell voltage criteria and the Sokolow-Lyon criteria, ST deviation and corrected QT interval) to determine the correlation. RESULTS: The QRS duration, left ventricular hypertrophy using the Cornell voltage criteria and the Sokolow-Lyon criteria and corrected QT interval exhibited significant correlation between the two types of electrocardiograms (correlation coefficient 0.878, 0.630, 0.770 and 0.847, respectively with P values of 0.01, 0.003, 0.01 and 0.01, respectively). ST deviation in V1 was weakly correlated between the two types of electrocardiograms without statistical significance (correlation coefficient 0.360 with a P value of 0.119). CONCLUSIONS: Our newly developed wireless 9-lead electrocardiogram demonstrated significant correlations with a conventional 12-lead electrocardiogram in terms of QRS duration, left ventricular hypertrophy and corrected QT interval.

Commonly consumed beverages in daily life: do they cause atrial fibrillation?

Atrial fibrillation (AF) is the most prevalent cardiac arrhythmia in the United States and worldwide. Caffeine, alcohol, and, more recently, energy drinks are the most commonly consumed beverages in daily living, especially by young individuals. Several questions have been raised about the implications of caffeine, alcohol, and energy drinks in cardiovascular health, especially in triggering AF. This review focuses on the role of these commonly consumed beverages as a cause of AF, with special emphasis of potential mechanisms and studies addressing this issue.

Intravenous vasodilator therapy in congestive heart failure.

The prevalence of congestive heart failure (CHF) is increasing in the US and worldwide, partly because patients are living longer. Treatment of CHF is mostly on an outpatient basis, but inpatient care is required for decompensated CHF, acute CHF or poor response to outpatient treatment. Control of symptoms is usually achieved by diuresis. Intravenous (IV) vasodilators are an important adjunct to the inpatient treatment of CHF. They work mainly by reducing the afterload on the myocardium although preload reduction also occurs. After clinical stabilisation, the goal is to switch to a maintenance oral regimen to be continued as outpatient therapy. The range of IV vasodilators available for inpatient treatment of CHF includes nitrates, phosphodiesterase inhibitors, dobutamine, morphine, ACE inhibitors, B-type natriuretic peptides and endothelin receptor antagonists. As each agent may have a different mechanism or site of action, each agent may affect preload, contractility or afterload to a different extent and it may be desirable to choose one over the other in a particular clinical setting. Examples of standard therapy include dobutamine, milrinone and nitroglycerin. Nesiritide, a B-type natriuretic peptide, is a newer vasodilator and US FDA approved for use in acute CHF. However, most studies with this agent have been in small numbers of patients with anecdotal findings. Larger studies are warranted to pinpoint the efficacy and adverse effects of this agent. It is primarily used to reduce the acuity of decompensated CHF on admission to hospital.Endothelin receptor antagonists show promise in the management of acute CHF, but continue to be investigational. Long-term data on their efficacy and safety are limited. None of the endothelin receptor antagonists are FDA approved for use in patients with CHF.

Novel anticoagulants vs warfarin for stroke prevention in atrial fibrillation.

Warfarin has remained the mainstay of stroke prevention in atrial fibrillation for the past 60 years. Recently, two new groups of novel oral anticoagulants- direct thrombin inhibitors (dabigatran) and factor Xa inhibitors (rivaroxaban, apixaban, edoxaban) have shown promising results in well conducted clinical trials in terms of efficacy, safety and convenience of usage. However, in real world practice these novel agents come with their share of side effects and drawbacks which the prescribing physician must be aware about. In this review we discuss the role of these novel agents in real world clinical practice - their advantages, disadvantages and future directions.

Antithrombotics in atrial fibrillation and coronary disease.

Atrial fibrillation (AF) is the most prevalent cardiac arrhythmia and approximately 18-45% of AF patients have concomitant coronary artery disease (CAD). Several studies have demonstrated that oral anticoagulation is the mainstay of therapy for stroke prevention in AF. Similarly, antiplatelet therapy including aspirin and P2Y12 inhibitor is recommended in the management of acute coronary syndrome and stable CAD. Despite the high prevalence of CAD with AF, practice guidelines are scarce on the appropriate antithrombotic regimen due to lack of large-scale randomized clinical trials. The use of direct thrombin and factor Xa inhibitors for stroke prevention in AF has also complicated the possible combinations of antithrombotic therapies. This review aims to discuss the available evidence regarding aspirin as an antithrombotic strategy, the role of novel anticoagulants and the specific clinical situations where aspirin may be beneficial in patients with AF and CAD.

Prognostic implications of diastolic dysfunction in patients with acute pulmonary embolism.

BACKGROUND: A history of congestive heart failure has been used to determine the prognosis in patients with acute pulmonary embolism. Diastolic dysfunction is responsible for the half of congestive heart failure but has not been understood well. METHODS: A total of 205 patients were reported admitted with acute pulmonary embolism from January 2009 to July 2011. We excluded hemodynamically unstable patients who received thrombolytics or underwent thromboembolectomy. We included hemodynamically stable patients who underwent echocardiogram within 72 hours of diagnosis. We reviewed medical records of 107 patients to investigate whether diastolic dysfunction increases in-hospital mortality or adverse clinical outcomes. RESULTS: Out of 107 patients, 10 patients died during hospitalization with in-hospital mortality rate of 9.3%. Among 84 patients without diastolic dysfunction as assessed by echocardiogram, six patients died with in-hospital mortality rate of 7.1%. Meanwhile, among 23 patients with diastolic dysfunction, four patients died with in-hospital mortality rate of 17.4%. The multivariable adjusted odds ratio was calculated as 2.71, with 95% confidence interval of 0.59 - 12.44. CONCLUSIONS: For hemodynamically stable patients with acute pulmonary embolism, diastolic dysfunction as assessed by echocardiogram could increase in-hospital mortality 2.71 fold, although this was not statistically significant. Further study with a large patient population is needed to determine the statistically significant implications of diastolic dysfunction in patients with acute pulmonary embolism.

Standardization of QRS duration measurement and LBBB criteria in CRT trials and clinical practice.

Based on the clinical trials so far, there is a major controversy regarding the benefit of CRT in patients with QRS≤150 milliseconds. Some studies have shown that a fair number of patients with QRS≤150 milliseconds benefit from CRT and it is needless to say that careful attention should be paid to CRT non-responders considering the risk of complications and cost-benefit ratio. Lack of uniformity in QRS measurement in all these trials could have a major influence on variable study outcomes. This is of concern because when the QRS is close to 120 milliseconds in patients with NYHA class III/IV symptoms or QRS close to 150 milliseconds in NYHA class I/II patients, the decision to recommend CRT implantation or undertake further risk stratification investigations is critically dependent on the EKG interpretation. In this paper we intent to raise the important question for need of standardized electrocardiographic criteria (QRS measurement and LBBB) in patients enrolled in CRT trials considering the variability in study results, high rates of CRT non response in the eligible population and the associated health care cost burden.

Atrial fibrosis: a risk stratifier for atrial fibrillation.

Atrial fibrillation (AF), especially persistent and long-standing persistent AF, may result in electro-anatomical changes in the left atrium, resulting in remodeling and deposition of fibrous tissue. There are emerging data that atrial substrate modification may increase the risk of thromboembolic complications, including stroke. Several studies have reported that atrial fibrosis is due to complex interactions among several cellular and neurohumoral mediators. Late gadolinium enhancement MRI has been reported to allow quantitative assessment of myocardial fibrosis in patients at risk of developing a stroke. Current stroke risk stratification criteria for AF do not utilize atrial fibrosis as an independent risk factor despite its association with AF and stroke. Further research is required in developing adequate risk stratification tools for predicting the stroke risk and catheter ablation outcomes in AF.