BACKGROUND:The American College of Cardiology has called for greater emphasis on patient-centered care, but methods to accomplish this goal have not yet been elucidated, particularly in training settings. This study examined the effect of providing fellow biographical information versus medical clinic information on perceptions of patient-centered care, patient-provider relationships, and medical visit engagement in a large, rural-serving cardiology training clinic. METHODS:Participating patients were assigned to receive either a biography about their cardiology fellow provider or information about the clinic facility. Participants completed questionnaires assessing their perceptions of patient-centered care and their relationship with their provider following the clinic visit. RESULTS:Participants (N=198; mean (M) age 62.72; 47.5% Black; 54.5% male) who received biographies perceived fellows as engaging in significantly higher levels of patient-centered care behavior (M: 74.54 versus 69.83, respectively, P=0.003). Moreover, the provider biography group reported significantly greater relationship depth with their providers (M: 26.72 versus 23.75, respectively, P=0.015) compared with controls, and were more likely to ask a question during their visit (96.9% versus 87%, respectively). CONCLUSIONS:Patients reported improved perceptions of patient-centered care and asked more questions when provided with fellow biographies. Biographical information about cardiology fellows may be a viable and low-cost method of improving perceptions of patient-centered care with minimal provider burden.

PURPOSE OF REVIEW:This paper reviews the unique processes and treatments of post-traumatic stress in implantable cardioverter-defibrillator (ICD) patients and posits specific clinical management recommendations.RECENT FINDINGS:PTSD is a common presenting problem for a prospective ICD patient and is a common response to ICD shocks. Approximately 32% of patients with sudden cardiac arrest report significant PTSD symptoms. Following ICD shock, approximately 20% experience PTSD from the shocks. Regardless, PTSD can interrupt and undermine clinical management from a cardiologist perspective and create significant disturbance in patients and families. Few cardiology clinics are outfitted to effectively manage psychological distress, in general, and PTSD, in particular. Effective management of PTSD patients can be achieved with both direct care in the cardiac clinic, as well as indirect care via multidisciplinary consultation and expertise. The importance of emotional validation, return to physical activity, and family engagement is emphasized in current management.

Introduction: Flecainide is a class 1c anti-arrhythmic agent that slows phase 0 of the fast inward sodium (Na) channels in a rate-dependent fashion leading to decreased conduction velocity in the His-Purkinje and ventricular myocardium. Its high affinity and slow unbinding prolong QRS duration on electrocardiogram (EKG). Partial renal excretion and a narrow therapeutic index of 0.2-1mcg/mL can cause drug toxicity. Case: A 72-year-old woman presented with palpitations and weakness. She had a history of non-ischemic cardiomyopathy, biventricular (BiV) implantable cardioverter defibrillator, frequent premature ventricular contractions on flecainide 100 mg twice a day, and chronic kidney disease. She was hypotensive and with acute kidney injury. EKG showed wide complex ventricular rhythm, QRS duration of 305 ms and intermittent ventricular pacing (Fig.1A), changed since EKG 6 months ago (Fig.1B). Device interrogation revealed normal sensing and impedances but failure to capture from all 3 leads. She had stable lead parameters and appropriate BiV pacing 6 months ago. Chest X ray showed stable lead positions. Flecainide toxicity was suspected, and Na bicarbonate infusion was started. Flecainide level was 2.4mcg/mL (normal <1mcg/mL). She went into an idioventricular rhythm which terminated spontaneously (Fig.1C). After 48 hours of Na bicarbonate infusion, lead capture was noted with narrower QRS (198 ms) (Fig.1D) and on day 6, EKG was back to effective BiV pacing with QRS duration 127 ms (Fig.1E). Discussion: This case highlights the EKG manifestations of flecainide toxicity including QRS widening, sine-wave pattern and loss of pacing capture due to prolonged ventricular refractoriness. It also underscores the reversibility of this condition with prompt treatment using Na bicarbonate. Conclusion: Early recognition and rapid treatment of the cardiac effects of flecainide toxicity is critical in managing a life threatening but reversible medical condition.

Cardiac thrombus, the most common intracardiac mass, is typically seen in the left side of the heart in the presence of atrial fibrillation, mitral stenosis, or impaired global wall motion. Right atrial thrombus, which is rarer, is usually associated with central venous catheter placement or pulmonary embolism. We present the case of a 24-year-old woman with a history of mitral valve prolapse who presented with fatigue and palpitations. Echocardiograms and cardiac magnetic resonance images revealed a right atrial mass compatible with a myxoma. However, after surgical excision of this and a second mass discovered intraoperatively, pathologic evaluation confirmed organized thrombus rather than myxoma. The patient's only risk factor was her use of oral contraceptive pills. Test results for hypercoagulable disorders revealed the presence of antiphosphatidylserine, an uncommon antiphospholipid antibody. The patient stopped taking the contraceptive. This case suggests the need to examine further the role of antiphosphatidylserine antibodies in the diagnosis of antiphospholipid syndrome.

Key Teaching Points•Left ventricular false tendons (LVFTs) are endocavitary structures in the ventricle that comprise fibrous tissue, myocardial fibers, blood vessels, and Purkinje fibers. Premature ventricular complexes (PVCs) originating from LVFTs may be due to the increased automaticity of Purkinje cells within muscle fibers or increased excitability owing to mechanical traction at the false tendon attachment site.•PVC triggering ventricular fibrillation (VF) storm is a true electrophysiological emergency and prompts careful evaluation. Treatment of PVC-triggered VF in patients without structural heart disease should first be aimed at studying and promptly removing any reversible proarrhythmic cause, like myocardial ischemia, electrolyte imbalances, QT-prolonging drugs, and inflammation.•Radiofrequency ablation with an intracardiac echocardiography–guided electroanatomical approach should be considered in patients with PVCs originating from LVFTs to improve the efficacy and safety by direct visualization of these dynamic endocavitary structures.•An implantable cardioverter-defibrillator is recommended for secondary prevention of sudden cardiac death in patients with idiopathic ventricular tachycardia/VF in the absence of reversible causes. •Left ventricular false tendons (LVFTs) are endocavitary structures in the ventricle that comprise fibrous tissue, myocardial fibers, blood vessels, and Purkinje fibers. Premature ventricular complexes (PVCs) originating from LVFTs may be due to the increased automaticity of Purkinje cells within muscle fibers or increased excitability owing to mechanical traction at the false tendon attachment site.•PVC triggering ventricular fibrillation (VF) storm is a true electrophysiological emergency and prompts careful evaluation. Treatment of PVC-triggered VF in patients without structural heart disease should first be aimed at studying and promptly removing any reversible proarrhythmic cause, like myocardial ischemia, electrolyte imbalances, QT-prolonging drugs, and inflammation.•Radiofrequency ablation with an intracardiac echocardiography–guided electroanatomical approach should be considered in patients with PVCs originating from LVFTs to improve the efficacy and safety by direct visualization of these dynamic endocavitary structures.•An implantable cardioverter-defibrillator is recommended for secondary prevention of sudden cardiac death in patients with idiopathic ventricular tachycardia/VF in the absence of reversible causes.

Background: Isthmus-dependent counterclockwise or clockwise flutter is well defined and responsive to radiofrequency ablation (RFA) of the cavotricuspidisthmus (CTI). However, inter-atrial septal (IAS) flutter is rare and occurs with IAS substrate abnormalities and prior cardiac surgery. Case: A 62-year-old female with paroxysmal AF on rivaroxaban, hypertension and diabetes mellitus presented with palpitations refractory to propafenone and metoprolol. She underwent successful isolation of all four pulmonary veins (PVs) and RFA of the CTI with demonstration of bidirectional block. A year later, she presented with atypical AFL (Fig 1A) failing cardioversion. During redo ablation, bipolar voltage map of the left atrium (LA) demonstrated durable isolation of all four PVs. Burst pacing (BP) from the coronary sinus (CS) up to 220ms did not induce AFL. The LA posterior box was isolated by creating a roof line and a line connecting the inferior veins (Fig 1B). No extra-PV triggers were noted on high dose isoproterenol. However, during the washout period, BP from the CS induced AFL with a tachycardia cycle length of 237ms, concentric CS activation and almost simultaneous activation along the crista in the right atrium (RA). High-density activation and coherent mapping of LA and RA suggested a micro-reentrant circuit over the posterior IAS with wavefront collision across the CTI (Fig 1C, D). Concealed entrainment was observed over the LA posterior septum near the transseptal puncture site. RFA successfully terminated the AFL. RFA was performed in a sequential unipolar fashion on both sides of the septum over areas of fractionation. No atrial arrhythmias were inducible with BP on or off isoproterenol. Patient remained in sinus rhythm at 9 month follow up. Conclusion: IAS flutter post AF ablation or cardiac surgery is rare, and management is challenging. While RFA has a 93% success rate, larger studies are required to further delineate this condition.

BACKGROUND Cryoballoon ablation（CBA） is recommended for patients with paroxysmal atrial fibrillation（AF） refractory to antiarrhythmic drugs. However, only 80% of patients benefit from initial CBA. There is growing evidence that pretreatment with angiotensin-converting enzyme inhibitors（ACEIs） and angiotensin receptor blockers（ARBs） decreases the recurrence of AF postablation, particularly in nonparoxysmal AF undergoing radiofrequency ablation. The role of ACEIs and ARBs in patients with paroxysmal AF in CBA remains unknown. We decided to investigate the role of ACEIs and ARBs in preventing the recurrence of atrial arrhythmia（AA） following CBA for paroxysmal AF.AIM To investigate the role of ACEIs and ARBs in preventing recurrence of AA following CBA for paroxysmal AF.METHODS We followed 103 patients（age 60.6 ± 9.1 years, 29% women） with paroxysmal AF undergoing CBA 1-year post procedure. Recurrence was assessed by documented AA on electrocardiogram or any form of long-term cardiac rhythm monitoring. A multivariable Cox proportional hazard model was used to assess if ACEI or ARB treatment predicted the risk of AA recurrence.RESULTS After a 1-year follow-up, 19（18.4%） participants developed recurrence of AA. Use of ACEI or ARB therapy was noted in the study population. Patients on ACEI/ARB had a greater prevalence of hypertension and coronary artery disease. On a multivariate model adjusted for baseline demographics and risk factors for AF, ACEI or ARB therapy did not prevent recurrence of AA following CBA（P = 0.72）. Similarly, on Kaplan–Meier analysis pretreatment with ACEI/ARB did not predict the time to first recurrence of AA（P = 0.2173）.CONCLUSION In our study population, preablation treatment with an ACEI or ARB had no influence on the recurrence of AA following CBA for paroxysmal AF.

COPD often coexists with HFpEF, but its impact on cardiovascular structure and function in HFpEF is incompletely understood. We aimed to compare cardiovascular phenotypes in patients with Chronic Obstructive Pulmonary Disease (COPD), Heart Failure with Preserved Ejection Fraction (HFpEF), or both. We studied 159 subjects with COPD alone (n = 48), HFpEF alone (n = 79) and HFpEF + COPD (n = 32). We used MRI and arterial tonometry to assess cardiac structure and function, thoracic aortic stiffness, and measures of body composition. Relative to participants with COPD only, those with HFpEF with or without COPD exhibited a greater prevalence of female sex and obesity, whereas those with HFpEF + COPD were more often African-American. Compared to the other groups, participants with HFpEF and COPD demonstrated a more concentric LV geometry (LV wall-cavity ratio 1.2, 95%CI: 1.1-1.3; p = 0.003), a greater LV mass (67.4, 95%CI: 60.7-74.2; p = 0.03, and LV extracellular volume (49.4, 95%CI: 40.9-57.9; p = 0.002). Patients with comorbid HFpEF + COPD also exhibited greater thoracic aortic stiffness assessed by pulse-wave velocity (11.3, 95% CI: 8.7-14.0 m/s; p = 0.004) and pulsatile load imposed by the ascending aorta as measured by aortic characteristic impedance (139 dsc; 95%CI=111-166; p = 0.005). Participants with HFpEF, with or without COPD, exhibited greater abdominal and pericardial fat, without difference in thoracic skeletal muscle size. In conclusion, individuals with co-morbid HFpEF and COPD have a greater degree of systemic large artery stiffening, LV remodeling, and LV fibrosis than those with either condition alone.

Paradoxical coronary artery embolism is often an underdiagnosed cause of acute myocardial infarction (MI). It should always be considered in patient with acute MI and a low risk profile for atherosclerotic coronary artery disease. We describe a patient with simultaneous acute saddle pulmonary embolism (PE) and acute ST segment elevation MI due to paradoxical coronary artery embolism. Transoesophageal echocardiography demonstrated a patent foramen ovale with right to left shunt and large saddle PE in the main pulmonary artery and coronary angiography demonstrated acute thrombotic occlusion of the right coronary artery.

Background: Cryoballoon ablation (CBA) is recommended for patients with paroxysmal atrial fibrillation (AF) refractory to anti-arrhythmic drugs. However, only 70% of patients benefit from an initial CBA. There is a growing evidence that pretreatment with angiotensin converting enzyme inhibitors (ACE-I) and angiotensin receptor blocker (ARB) decreases recurrence of AF post ablation, particularly in non-paroxysmal AF undergoing radiofrequency ablation. The role of ACE-I and ARB in patients with paroxysmal AF in CBA remains unknown. We decided to investigate the role of ACE-I and ARB in preventing recurrence of atrial arrhythmias (AA) following CBA for paroxysmal AF. Methods: We followed 103 patients (Age 60.6 ± 9.1, 29% women) with paroxysmal AF undergoing CBA for one year post procedure. Recurrence was assessed by documented AA on EKG or any form of long-term cardiac rhythm monitoring. A multivariable cox proportional hazard model was used to assess if ACE-I or ARB treatment predicted risk of AA recurrence. Results: After a one year follow up, 19 (18.4%) participants developed recurrence of AA. Use of ACE-I or ARB therapy was noted in the study population. Patients on ACE-I/ARB had a greater prevalence of hypertension and coronary artery disease. On a multivariate model adjusted for baseline demographics and risk factors for AF, ACEI or ARB therapy did not prevent recurrence of AA following CBA (Table, p=0.72). Similarly, on Kaplan-Meier analysis pretreatment with ACE-I/ARB did not predict time to first recurrence of AA (Figure, p=0.2173). Conclusion: In our study population pre-ablation treatment with an ACE-I or an ARB had no influence on the recurrence of AA following CBA for paroxysmal AF.

It is unknown whether obesity modifies the effect of obstructive sleep apnea (OSA) and positive airway pressure (PAP) therapy on cardiac remodeling and NT-proBNP (N-terminal pro-B-type natriuretic peptide) levels. We compared NT-proBNP and cardiac magnetic resonance imaging in adults without OSA (n=56) and nonobese (n=73; body mass index <30 kg/m 2 ) and obese (n=136; body mass index ≥30 kg/m 2 ) adults with OSA. We also investigated these traits in nonobese (n=45) and obese (n=78) participants with OSA adherent to 4 months of PAP treatment. At baseline, left ventricular mass to end-diastolic volume ratio, a measure of left ventricular concentricity, was greater in both nonobese and obese participants with OSA compared with those without OSA. Participants with OSA and obesity exhibited reduced phasic right atrial function. No significant differences in baseline NT-proBNP were observed across groups. The effect of PAP treatment on NT-proBNP and left atrial volume index was significantly modified by obesity. In nonobese participants, PAP therapy was associated with a decrease in NT-proBNP ( P <0.0001) without a change in left atrial volume index, whereas in obese participants, PAP was associated with an increase in left atrial volume index ( P =0.006) without a change in NT-proBNP. OSA was associated with left ventricular concentric remodeling independent of obesity and right atrial dysfunction in participants who were obese. PAP treatment was associated with reduced NT-proBNP in nonobese participants with OSA, but left atrial enlargement in obese participants with OSA, suggesting that PAP-induced reduction in BNP release (which is known to occur during obstructive apnea episodes) may lead to volume retention in obese participants with OSA. Registration: URL: https://www.clinicaltrials.gov ; Unique identifier: NCT01578031.