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1.  Combined Right Ventricular Outflow Tract Epicardial and Endocardial Late Potential Ablation for Treatment of Brugada Storm: A Case Report and Review of the Literature 
Cardiology and Therapy  2016;5(2):229-243.
A 34-year-old man with Brugada syndrome (BrS) presented with electrical storm, manifested as multiple appropriate shocks from his implantable cardioverter-defibrillator over a period of 7 hours. He had not tolerated prior treatment with quinidine, and had self-discontinued cilostazol citing persistent palpitations. After stabilization with intravenous isoproterenol, an electrophysiology study was performed but no spontaneous or induced ventricular ectopic beats were identified. A three-dimensional (3D) endocardial electro-anatomic map of the right ventricular outflow tract (RVOT), pulmonic valve, and pulmonary artery, as well as a 3D epicardial map of the RVOT, were created. Low voltage, complex, fractionated electrograms and late potentials were targeted for irrigated radiofrequency ablation both endocardially and epicardially. Post-procedure, he was maintained on cilostazol (referring clinician preference), and has had no further ventricular tachyarrhythmia episodes over the past forty-one months. We propose that this novel ablation strategy may be useful for acute management of selected patients with BrS.
PMCID: PMC5125114  PMID: 27646458
Brugada syndrome; Implantable cardioverter-defibrillator; Late potentials; Radiofrequency ablation
2.  L-Type Calcium Channels Do Not Play a Critical Role in Chest Blow Induced Ventricular Fibrillation: Commotio Cordis 
Cardiology Research and Practice  2016;2016:5191683.
Background. In a commotio cordis swine model, ventricular fibrillation (VF) can be induced by a ball blow to the chest believed secondary to activation of mechanosensitive ion channels. The purpose of the current study is to evaluate whether stretch induced activation of the L-type calcium channel may cause intracellular calcium overload and underlie the VF in commotio cordis. Method and Results. Anesthetized juvenile swine received 6 chest wall strikes with a 17.9 m/s lacrosse ball timed to the vulnerable period for VF induction. Animals were randomized to IV verapamil (n = 6) or placebo (n = 6). There was no difference in the observed frequency of VF between verapamil (19/26: 73%) and placebo (20/36: 56%) treated animals (p = 0.16). There was also no significant difference in the combined endpoint of VF or nonsustained VF (21/26: 81% in verapamil versus 24/36: 67% in controls, p = 0.22). Conclusions. In this experimental model of commotio cordis, verapamil did not prevent VF induction. Thus, in commotio cordis it is unlikely that stretch activation of the L-type calcium channel with resultant intracellular calcium overload plays a prominent role.
PMCID: PMC4746352  PMID: 26925288
3.  Advanced Anderson-Fabry disease presenting with left ventricular apical aneurysm and ventricular tachycardia 
A 54-year-old female with Anderson-Fabry disease (AFD)-R342Q missense mutation on exon 7 in alpha-galactosidase A (GLA) gene - presented with sustained ventricular tachycardia. Imaging confirmed the presence of a new left ventricular apical aneurysm (LVAA) and a significantly reduced intra-cavitary gradient compared to two years prior. AFDcv is an X-linked lysosomal storage disorder caused by GLA enzyme deficiency. The phenotypic expression of AFD in the heart is not well described. Cardiac involvement can include left ventricular hypertrophy (LVH), which is typically symmetric, but can also mimic hypertrophic cardiomyopathy (HCM). Left ventricular apical aneurysm is a rare finding in HCM. We suggest a shared mechanism of LVAA formation in AFD and HCM, independent of the underlying cardiomyopathy. Mechanisms of LVAA formation in HCM include genetic predisposition and long-standing left ventricular wall stress from elevated intra-cavitary systolic pressures due to mid-cavitary obstruction. Both mechanisms are supported in this patient (a brother with AFD also developed a small LVAA). Screening for AFD should be considered in cases of unexplained LVH, particularly in patients with the aneurysmal variant of HCM.
PMCID: PMC4468899  PMID: 26090373
Anderson-Fabry disease; Sustained ventricular tachycardia; Left ventricular apical aneurysm; Hemodynamic compensation; Transthoracic echocardiography; Magnetic resonance imaging; Hypertrophic cardiomyopathy
4.  Ventricular Tachycardia Associated with Radiation-Induced Cardiac Sarcoma 
Texas Heart Institute Journal  2014;41(6):620-625.
Cardiac tumors can lead to distinct electrocardiographic changes and ventricular arrhythmias. Benign and malignant cardiac tumors have been associated with ventricular tachycardia. When possible, benign tumors should be resected when ventricular arrhythmias are intractable. Chemotherapy can shrink malignant tumors and eliminate arrhythmias.
We report the case of a 52-year-old woman with breast sarcoma whom we diagnosed with myocardial metastasis after she presented with palpitations. The initial electrocardiogram revealed sinus rhythm with new right bundle branch block and ST-segment elevation in the anterior precordial leads. During telemetry, hemodynamically stable, sustained ventricular tachycardia with right ventricular localization was detected. Images showed a myocardial mass in the right ventricular free wall. Amiodarone suppressed the arrhythmia.
To our knowledge, this is the first report of ventricular tachycardia associated with radiation-induced undifferentiated sarcoma. We discuss the distinct electrocardiographic changes and ventricular arrhythmias that can be associated with cardiac tumors, and we review the relevant medical literature.
PMCID: PMC4251334  PMID: 25593527
Amiodarone/administration & dosage/adverse effects/therapeutic use; arrhythmias, cardiac/diagnosis; heart neoplasms/complications/radiotherapy/secondary; neoplasms, radiation-induced/therapy; tachycardia, ventricular/diagnosis/drug therapy/etiology/physiopathology/prevention & control
5.  Short-Term Effects of Ketamine and Isoflurane on Left Ventricular Ejection Fraction in an Experimental Swine Model 
ISRN Cardiology  2011;2011:582658.
Background. General anesthesia is an essential element of experimental medical procedures. Ketamine and isoflurane are agents commonly used to induce and maintain anesthesia in animals. The cardiovascular effects of these anesthetic agents are diverse, and the response of global myocardial function is unknown. Methods. In a series of 15 swine, echocardiography measurements of left ventricular ejection fraction (LVEF) were obtained before the animals received anesthesia (baseline), after an intramuscular injection of ketamine (postketamine) and after inhaled isoflurane (postisoflurane). Results. The mean LVEF of an unanesthetized swine was 47 ± 3%. There was a significant decrease in the mean LVEF after administration of ketamine to 41 + 6.5% (P = 0.003). The addition of inhaled isoflurane did not result in further decrease in mean LVEF (mean LVEF 38 ± 7.2%, P = 0.22). Eight of the swine had an increase in their LVEF with sympathetic stimulation. Conclusions. In our experimental model the administration of ketamine was associated with decreased LV function. The decrease may be largely secondary to a blunting of sympathetic tone. The addition of isoflurane to ketamine did not significantly change LV function. A significant number of animals had returned to preanesthesia LV function with sympathetic stimulation.
PMCID: PMC3262505  PMID: 22347646
6.  Relation of Different Measures of Low-Density Lipoprotein Cholesterol to Risk of Coronary Heart Disease and Death in a Meta-Regression Analysis of Large-Scale Trials of Statin Therapy 
The American journal of cardiology  2010;105(9):1289-1296.
Multiple randomized controlled trials (RCTs) have established the efficacy of statins for prevention of cardiovascular disease. The benefits observed are often framed in terms of percent reductions in low-density lipoprotein cholesterol (LDL-C) from baseline or percent reduction between control and treatment groups, even though epidemiological data suggest that absolute inter-group difference in LDL-C (ΔLDLControl-Rx) is the more informative measure. We conducted a systematic review of large-scale trials of statins versus placebo, usual care or active (lower-dose statin) control to calculate updated summary estimates of risk reduction in coronary heart disease (CHD) and all-cause mortality. Meta-regression analysis was used to ascertain the relations of different LDL-C metrics to outcome. In 20 eligible RCTs, there were significant overall reductions for CHD (OR=0.72, 95% CI=0.67–0.78) and mortality (OR=0.89, 95% CI=0.84–0.94), but with substantial variability in trial results. ΔLDLControl-Rx was the strongest determinant of CHD risk reduction, particularly after excluding active-comparator studies, and was independent of baseline LDL-C. By contrast, baseline LDL-C edged ΔLDLControl-Rx as the strongest determinant of mortality, but neither was significant after exclusion of active-comparator studies. Exclusion of 3 RCTs involving distinct populations, however, rendered ΔLDLControl-Rx the predominant determinant of mortality reduction. In conclusion, these findings underscore the primacy of absolute reductions in LDL-C to the design and interpretation of RCTs of lipid-lowering therapies, and to framing treatment recommendations based on the proven coronary benefits of these drugs.
PMCID: PMC2917836  PMID: 20403481
7.  Role of SREBP-1 in the Development of Parasympathetic Dysfunction in the Hearts of Type I Diabetic Akita Mice 
Circulation research  2009;105(3):287-294.
Diabetic Autonomic Neuropathy (DAN), a major complication of diabetes mellitus, is characterized in part by impaired cardiac parasympathetic responsiveness. Parasympathetic stimulation of the heart involves activation of an acetylcholine-gated K+ current, IKAch, via a (GIRK1)2/(GIRK4)2 K+ channel. Sterol regulatory element binding protein-1 (SREBP-1) is a lipid-sensitive transcription factor. We describe a unique SREBP-1-dependent mechanism for insulin regulation of cardiac parasympathetic response in a mouse model for DAN. Compared to WT mice, Ins2Akita type I diabetic mice demonstrated a decrease in the negative chronotropic response to carbamylcholine characterized by a 2.4 fold decrease in duration of bradycardia; a 52±8% decrease in atrial expression of GIRK1 (P<0.01) and a 31.3±2.1% decrease in SREBP-1 (P<0.05). Myocytes from atria of Akita mice exhibited a markedly decreased carbamylcholine stimulation of IKAch with a peak value of −181±31 pA/pF compared to −451±62 pA/pF (P<0.01) for cells from WT mice. Insulin treatment of Akita mice reversed the impairment in parasympathetic response, increased the expression of GIRK1, SREBP-1 and IKAch activity in atrial myocytes from these mice to levels in WT mice. Insulin treatment of cultured atrial myocytes stimulated GIRK1 expression 2.68±0.12 fold (P<0.01) while overexpression of DN-SREBP-1 reversed this insulin effect. Finally, adenoviral expression of SREBP-1 in Akita atrial myocytes reversed the impaired IKAch to levels in cells from WT. These results support a unique molecular mechanism for insulin regulation of GIRK1 expression and parasympathetic response via SREBP-1 which might play a role in the pathogenesis of DAN in response to insulin deficiency in the diabetic heart.
PMCID: PMC2730600  PMID: 19423844
Diabetic autonomic neuropathy; SREBP; insulin deficiency; GIRK channel
8.  Parasympathetic response in chick myocytes and mouse heart is controlled by SREBP 
Parasympathetic stimulation of the heart, which provides protection from arrhythmias and sudden death, involves activation of the G protein–coupled inward rectifying K+ channel GIRK1/4 and results in an acetylcholine-sensitive K+ current, IKACh. We describe a unique relationship between lipid homeostasis, the lipid-sensitive transcription factor SREBP-1, regulation of the cardiac parasympathetic response, and the development of ventricular arrhythmia. In embryonic chick atrial myocytes, lipid lowering by culture in lipoprotein-depleted serum increased SREBP-1 levels, GIRK1 expression, and IKACh activation. Regulation of the GIRK1 promoter by SREBP-1 and lipid lowering was dependent on interaction with 2 tandem sterol response elements and an upstream E-box motif. Expression of dominant negative SREBP-1 (DN–SREBP-1) reversed the effect of lipid lowering on IKACh and GIRK1. In SREBP-1 knockout mice, both the response of the heart to parasympathetic stimulation and the expression of GIRK1 were reduced compared with WT. IKACh, attenuated in atrial myocytes from SREBP-1 knockout mice, was stimulated by SREBP-1 expression. Following myocardial infarction, SREBP-1 knockout mice were twice as likely as WT mice to develop ventricular tachycardia in response to programmed ventricular stimulation. These results demonstrate a relationship between lipid metabolism and parasympathetic response that may play a role in arrhythmogenesis.
PMCID: PMC2104475  PMID: 18060044
9.  Commotio Cordis 
Sudden arrhythmic death as a result of a blunt chest wall blow has been termed Commotio Cordis (CC). CC is being reported with increasing frequency with more than 180 cases now described in the United States Commotio Cordis Registry. The clinical spectrum is diverse; however young athletes tend to be most at risk, with victims commonly being struck by projectiles regarded as standard implements of the sport. Sudden death is instantaneous and victims are most often found in ventricular fibrillation (VF). Chest blows are not of sufficient magnitude to cause any significant damage to overlying thoracic structures and autopsy is notable for the absence of any structural cardiac injury. Development of an experimental model has allowed for substantial insights into the underlying mechanisms of sudden death. In anesthetized juvenile swine, induction of VF is instantaneous following chest impacts that occur during a vulnerable window before the T wave peak. Other critical variables, including the impact velocity and location, and the hardness of the impact object have also been identified. Rapid left ventricular pressure rise following chest impact likely results in activation of ion channels via mechano-electric coupling. The generation of inward current through mechano-sensitive ion channels results in augmentation of repolarization and non-uniform myocardial activation, and is the cause of premature ventricular depolarizations that are triggers of VF in CC. Currently available chest protectors commonly used in sport are not adequately designed to prevent CC. The development of more effective chest protectors and the widespread availability of automated external defibrillators at youth sporting events could improve the safety of young athletes.
PMCID: PMC2018736  PMID: 17957272
Commotio cordis; Ventricular Fibrillation; Athletes; Sudden Death; Mechano-electric coupling

Results 1-9 (9)