Prakriti Gaba

Percutaneous Pericardial Resection: A Novel Potential Treatment for Heart Failure with Preserved Ejection Fraction

Background— People with heart failure and preserved ejection fraction develop increases in left ventricular (LV) end-diastolic pressures during exercise that contribute to dyspnea. In normal open-chest animal preparations, the pericardium restrains LV filling when central blood volume increases. We hypothesized that resection of the pericardium using a minimally invasive epicardial approach would mitigate the increase in LV end-diastolic pressure that develops during volume loading in normal and diseased hearts with the chest intact. Methods and Results— Invasive hemodynamic assessment was performed at baseline and after saline load before and after pericardial resection in normal canines with open (n=3) and closed chest (n=5) and in a pig model with features of human heart failure and preserved ejection fraction with sternum intact (n=4). In closed-chest animals, pericardiotomy was performed using a novel subxiphoid procedure. In both experimental preparations of normal dogs, pericardiotomy blunted the increase in LV end-diastolic pressure with saline infusion, while enhancing the saline-mediated increase in LV end-diastolic volume. With chest intact in the pig model, percutaneous pericardial resection again blunted the increase in LV end-diastolic pressure secondary to volume expansion (+4±3 versus +13±5 mm Hg; P =0.014), while enhancing the saline-mediated increase in LV end-diastolic volume (+17±1 versus +10±2 mL; P =0.016). Conclusions— This proof of concept study demonstrates that pericardial resection through a minimally invasive percutaneous approach mitigates the elevation in LV filling pressures with volume loading in both normal animals and a pig model with diastolic dysfunction. Further study is warranted to determine whether this method is safe and produces similar acute and chronic hemodynamic benefits in people with heart failure and preserved ejection fraction.Background— People with heart failure and preserved ejection fraction develop increases in left ventricular (LV) end-diastolic pressures during exercise that contribute to dyspnea. In normal open-chest animal preparations, the pericardium restrains LV filling when central blood volume increases. We hypothesized that resection of the pericardium using a minimally invasive epicardial approach would mitigate the increase in LV end-diastolic pressure that develops during volume loading in normal and diseased hearts with the chest intact. Methods and Results— Invasive hemodynamic assessment was performed at baseline and after saline load before and after pericardial resection in normal canines with open (n=3) and closed chest (n=5) and in a pig model with features of human heart failure and preserved ejection fraction with sternum intact (n=4). In closed-chest animals, pericardiotomy was performed using a novel subxiphoid procedure. In both experimental preparations of normal dogs, pericardiotomy blunted the increase in LV end-diastolic pressure with saline infusion, while enhancing the saline-mediated increase in LV end-diastolic volume. With chest intact in the pig model, percutaneous pericardial resection again blunted the increase in LV end-diastolic pressure secondary to volume expansion (+4±3 versus +13±5 mm Hg; P=0.014), while enhancing the saline-mediated increase in LV end-diastolic volume (+17±1 versus +10±2 mL; P=0.016). Conclusions— This proof of concept study demonstrates that pericardial resection through a minimally invasive percutaneous approach mitigates the elevation in LV filling pressures with volume loading in both normal animals and a pig model with diastolic dysfunction. Further study is warranted to determine whether this method is safe and produces similar acute and chronic hemodynamic benefits in people with heart failure and preserved ejection fraction.

Implantable cardioverter-defibrillator explantation for overdiagnosed or overtreated congenital long QT syndrome

BACKGROUND Primary treatment of long QT syndrome (LQTS) currently consists of beta-blocker therapy, although an implantable cardioverter-defibrillator (ICD) is considered for high-risk patients. However, both overdiagnosis and overtreatment must be avoided because their sequelae can be significant. OBJECTIVE The purpose of this study was to evaluate the prevalence and details of ICD explants in a cohort of patients from a tertiary genetic heart rhythm clinic for a previously rendered diagnosis of LQTS. METHODS Overall, 1227 consecutive patients were included in the study. All patients had been referred to the Mayo Clinic for evaluation of possible LQTS and subsequently were either diagnosed with LQTS or dismissed as normal. Further stratification of patients was conducted to assess how many patients had an ICD and how many had a subsequent ICD explant. RESULTS In total, 170 patients (14%) had an ICD, including 157 of 670 patients (23%) with confirmed LQTS and 13 of 557 patients (2%) who did not have LQTS. Among these, 12 of 1227 (1%) had the ICD removed: 7 of 157 LQTS patients (4.5%) compared to 5 of 14 non-LQTS patients (36%). Before explant, 5 of 12 patients (42%) experienced inappropriate shocks, ranging from 2 to as many as 54 shocks. In addition, 4 had a device-related infection, and 9 had device malfunction (including lead dysfunction or fracture). None of these patients had a breakthrough cardiac event since removal of their ICD during 5.5 ± 3.5 years of follow-up. CONCLUSION Implications of overdiagnosis and overtreatment are profound because unnecessary ICD placement can be associated with infection, malfunction, inappropriate shocks, and subsequent anxiety.

Clinical impact of delirium and antipsychotic therapy: 10-Year experience from a referral coronary care unit

Background: Little is known about safety of antipsychotic therapy for delirium in the coronary care unit (CCU). Our aim was to examine the effect of delirium and antipsychotic therapy among CCU patients. Methods and results: Pre-study Confusion Assessment Method-Intensive Care Unit (CAM–ICU) criteria were implemented in screening consecutive patients admitted to a referral CCU from 2004–2013. Death status was prospectively ascertained. Of 11,079 study patients, the incidence of delirium was 8.3% (n=925). Delirium was associated with an increased risk of in-hospital mortality (adjusted odds ratio (OR) 1.49; 95% confidence interval (CI), 1.08–2.08; p=0.02) and one-year mortality among patients who survived from CCU admission (adjusted hazard ratio (HR) 1.46; 95% CI, 1.12–1.87; p=0.005). A total of 792 doses of haloperidol (5 mg/day; interquartile range (IQR) 3–10) or quetiapine (25 mg/day; IQR 13–50) were given to 244 patients with delirium. The clinical characteristics of patients with delirium who did and did not receive antipsychotic therapy were not different (baseline corrected QT (QTc) interval 457±58 ms vs 459±60 ms, respectively; p=0.65). In comparison to baseline, mean QTc intervals after the first and third doses of the antipsychotics were not significantly prolonged in haloperidol (448±56, 458±57 and 450±50 ms, respectively) or quetiapine groups (470±66, 467±68 and 462±46 ms, respectively) (p>0.05 for all). Additionally, in-hospital mortality (adjusted OR 0.67; 95% CI, 0.42–1.04; p=0.07), ventricular arrhythmia (adjusted OR 0.87; 95% CI, 0.17–3.62; p=0.85) and one-year mortality among the hospital survivors (adjusted HR 0.86; 95% CI 0.62–1.17; p=0.34) were not different in patients with delirium irrespective of whether or not they received antipsychotics. Conclusion: In patients admitted to the CCU, delirium was associated with an increase in both in-hospital and one-year mortality. Low doses of haloperidol and quetiapine appeared to be safe, without an increase in risk of sudden cardiac death, in-hospital mortality, or one-year mortality in carefully monitored patients.

Association of Serum Magnesium on Mortality in Patients Admitted to the Intensive Cardiac Care Unit

BACKGROUND Although electrolyte disturbances may affect cardiac action potential, little is known about the association between serum magnesium and corrected QT (QTc) interval as well as clinical outcomes. METHODS A consecutive 8498 patients admitted to the Mayo Clinic Hospital-Rochester cardiac care unit (CCU) from January 1, 2004 through December 31, 2013 with 2 or more documented serum magnesium levels, were studied to test the hypothesis that serum magnesium levels are associated with in-hospital mortality, sudden cardiac death, and QTc interval. RESULTS Patients were 67 ± 15 years; 62.2% were male. The primary diagnoses for CCU admissions were acute myocardial infarction (50.7%) and acute decompensated heart failure (42.5%), respectively. Patients with higher magnesium levels were older, more likely male, and had lower glomerular filtration rates. After multivariate analyses adjusted for clinical characteristics including kidney disease and serum potassium, admission serum magnesium levels were not associated with QTc interval or sudden cardiac death. However, the admission magnesium levels ≥2.4 mg/dL were independently associated with an increase in mortality when compared with the reference level (2.0 to <2.2 mg/dL), having an adjusted odds ratio of 1.80 and a 95% confidence interval of 1.25-2.59. The sensitivity analysis examining the association between postadmission magnesium and analysis that excluded patients with kidney failure and those with abnormal serum potassium yielded similar results. CONCLUSION This retrospective study unexpectedly observed no association between serum magnesium levels and QTc interval or sudden cardiac death. However, serum magnesium ≥2.4 mg/dL was an independent predictor of increased hospital morality among CCU patients.

Beating Heart Validation of Safety and Efficacy of a Percutaneous Pericardiotomy Tool

Epicardial procedures frequently require pericardial manipulation. We aimed to develop a nonsurgical percutaneous pericardial modification tool that may (1) facilitate epicardial‐based procedures by enabling adhesiolysis or (2) attenuate the myocardial constraining effect of the pericardium.

Fascicular Ventricular Arrhythmias: Pathophysiologic Mechanisms, Anatomical Constructs, and Advances in Approaches to Management.

Ventricular arrhythmias involving the fascicular system may be seen in both structurally normal and abnormal hearts. Idiopathic fascicular ventricular tachycardia represents almost 10% to 15% of idiopathic ventricular tachycardia related to the left ventricle.1,2 Cohen et al3 and subsequently Zipes et al4 first described these arrhythmias in the 1970s as relatively narrow right bundle left axis arrhythmias that arose close to the posterior fascicle and could be induced with atrial pacing. Belhassen et al5 later described the responsiveness of these arrhythmias to verapamil. Although initial studies focused on arrhythmias related to the left posterior fascicle, it is possible for arrhythmias to arise from any portion of the fascicular system and in both structurally normal and abnormal hearts. Furthermore, when approaching the patient presenting with arrhythmias arising from the His-Purkinje system, it is important to consider the unique complexities related to mapping and ablation. In this review, we will focus on the mechanisms of such arrhythmias, relevant embryology, anatomy and physiology, and approaches to management in both the presence and absence of other structural heart disease. Broadly, fascicular ventricular tachycardia in the absence of other structural heart disease will be termed idiopathic fascicular ventricular tachycardia (IFVT), whereas that related to structural disease will be discussed in the context of the relevant disease state. Generally, IFVT is separated into 3 types—left posterior fascicular with a right bundle branch block pattern and left axis deviation, left anterior with a right bundle branch block and right axis deviation pattern, and left upper septal fascicular with a narrow QRS and normal axis but often with a right bundle branch block morphology. There are rare reported cases of left bundle branch block pattern, V3–V4 transition IFVT with a normal axis arising from the right bundle branch. In …

A Novel Defibrillation Tool: Percutaneously Delivered, Partially Insulated Epicardial Defibrillation

INTRODUCTION Epicardial defibrillation systems currently require surgical access. We aimed to develop a percutaneous defibrillation system with partially-insulated epicardial coils to focus electrical energy on the myocardium and prevent or minimize extra-cardiac stimulation. METHODS We tested 2 prototypes created for percutaneous introduction into the pericardial space via a steerable sheath. This included a partially-insulated defibrillation coil and a defibrillation mesh with a urethane balloon acting as an insulator to the face of the mesh not in contact with the epicardium. The average energy associated with a chance of successful defibrillation 75% of the time (ED75) was calculated for each experiment. RESULTS Of 16 animal experiments, 3 pig experiments had malfunctioning mesh prototypes such that results were unreliable; these were excluded. Therefore, 13 animal experiments were analyzed - 6 canines (29.8±4.0kg); 7 pigs (41.1±4.4kg). The overall ED75 was 12.8±6.7J (10.9±9.1J for canines; 14.4±3.9J in pigs [P=0.37]). The lowest ED75 obtained in canines was 2.5J while in pigs it was 9.5J. The lowest energy resulting in successful defibrillation was 2J in canines and 5J in pigs. There was no evidence of coronary vessel injury or trauma to extra-pericardial structures. CONCLUSION Percutaneous, epicardial defibrillation using a partially insulated coil is feasible and appears to be associated with low defibrillation thresholds. Focusing insulation may limit extra-cardiac stimulation and potentially lower energy requirements for efficient defibrillation.

Incidence of atypical nevi in Olmsted County: an epidemiological study.

The association of atypical nevi with melanoma and other forms of skin cancer has not been clearly defined.

Grinding to a halt: Stimulation of the trigeminal cardiac reflex from severe bruxism

Bruxism, which is reported in 8% of the population, can stimulate the trigeminal cardiac reflex and lead to profound vagal effects on the heart. Introduction The trigeminal cardiac reflex (TCR) is a unique, powerful, and well-established neurocardiogenic reflex that is a result of stimulation along the path of the fifth cranial nerve (trigeminal nerve). It can produce adverse cardiorespiratory changes including hypotension, bradycardia, and asystole, as well as gastric consequences such as hypermotility. This reflex has been reported to occur in various surgical conditions, as well as in neurosurgical interventions. Sleep bruxism, thought to be a more intense form of rhythmic masticatory muscle activity, has a prevalence of about 8% and has been explicitly linked to the TCR. We report a case of a young woman with severe bruxism who incited her TCR, which subsequently produced profound nocturnal pauses that ultimately required dual-chamber pacemaker implantation.

Right Ventricular Dysfunction and Long-Term Risk of Sudden Cardiac Death in Patients With and Without Severe Left Ventricular Dysfunction

Background: Right ventricular systolic dysfunction (RVD) often coexists with various cardiopulmonary diseases. However, the association between RVD and risk of sudden cardiac death (SCD) has not been well studied. This study examined the risk of SCD associated with RVD in patients with heterogeneous underlying cardiac diseases. Methods: The Mayo Clinic cardiac care unit database included 5463 consecutive patients with complete echocardiographic evaluation to assess right ventricular systolic function and RVD severity. Prospective surveillance follow-up was obtained for all patients. SCD was adjudicated when a malignant ventricular arrhythmia was documented as the primary rhythm leading to death. Results: The prevalence of mild RVD and moderate-severe RVD was 14.9% and 17.1%, respectively. Patients with RVD were more likely to have a history of congestive heart failure, cardiac arrest, pulmonary disease, and lower baseline left ventricular ejection fraction compared with those with normal right ventricular systolic function. During a median follow-up of 14 months, the incidence of SCD was highest in patients with moderate-severe RVD (7.4% versus 4.4% in mild RVD versus 1.6% in normal right ventricular function; P<0.001). After adjustment for baseline characteristics, mild RVD (adjusted hazard ratio, 1.57; P=0.046) and moderate-severe RVD (adjusted hazard ratio, 1.91; P=0.006) were independently associated with an increased risk of SCD. Moderate-severe RVD remained an independent predictor of SCD for patients with left ventricular ejection fraction >35% without or with preexisting implantable cardioverter-defibrillator (adjusted hazard ratio, 4.12; P=0.003 and adjusted hazard ratio, 5.04; P<0.001, respectively). Conclusions: Presence of RVD in patients with a history of preexisting cardiac disease is an independent predictor of SCD irrespective of left ventricular ejection fraction.