Download the Free Unbound MEDLINE PubMed App to your smartphone or tablet.
Available for iPhone, iPad, iPod touch, and Android.
Cardiovascular AND Tachycardia, ventricular, [keywords]
- Extracorporeal life support as rescue strategy for out-of-hospital and Emergency Department cardiac arrest. [JOURNAL ARTICLE]
- Resuscitation 2014 Sep 5.
Extracorporeal life support (ECLS) has been trialed as a rescue strategy for patients with cardiac arrest unresponsive to conventional cardiopulmonary resuscitation.We sought to describe our institution's experience with implementation of ECLS for out-of-hospital and Emergency Department (ED) cardiac arrests. Our primary outcome was survival to hospital discharge.Consecutive patients placed on ECLS in the ED or within one hour of admission after out-of-hospital or ED cardiac arrest were enrolled at two urban academic medical centers in the United States from July 2007-April 2014.During the study period, 26 patients were included. Average age was 40±15 years, 54% were male, and 42% were white. Initial cardiac rhythms were ventricular fibrillation or pulseless ventricular tachycardia in 42%. The average time from initial cardiac arrest to initiation of ECLS was 77±51minutes (range 12-180minutes). ECLS cannulation was unsuccessful in two patients. Eighteen (69%) had complications related to ECLS, most commonly bleeding and ischemic events. Four patients (15%) survived to discharge, three of whom were neurologically intact at 6 months.ECLS shows promise as a rescue strategy for refractory out-of-hospital or ED cardiac arrest but is not without challenges. Further investigations are necessary to refine the technique, patient selection, and ancillary therapeutics.
- Renewed impact of lidocaine on refractory ventricular arrhythmias in the amiodarone era. [JOURNAL ARTICLE]
- Int J Cardiol 2014 Aug 27.
Recent guidelines for treating ventricular fibrillation (VF) and ventricular tachycardia (VT) stress class III antiarrhythmic drugs, but some malignant arrhythmias refractory to these agents still occur in clinical practice. The possibility of a new treatment strategy involving lidocaine and amiodarone combination therapy was evaluated.From September 2008 to September 2013, 62 patients were treated at our hospital with lidocaine. The medical records were retrospectively reviewed. Twenty inappropriate patients were excluded. The remaining 42 patients were analyzed. Patients were divided into two groups according to the effectiveness of lidocaine in terminating refractory ventricular arrhythmias: the effective group.LVEF was significantly higher in the lidocaine effective (E) group compared to the ineffective (I) group (44±16% vs. 32±10%, p=0.027). There were more patients already on amiodarone at the start of lidocaine therapy in the E group compared to the I group (11/26 vs. 1/16, p=0.012). Furthermore, patients receiving lidocaine without amiodarone were re-analyzed to estimate the actual effect of lidocaine. Of the 30 patients not receiving amiodarone, 15 were in the effective without amiodarone (E w/o A) group and 15 were in the ineffective without amiodarone (I w/o A) group. LVEF was significantly higher in the E w/o A group than in the I w/o A group (51±16% vs. 32±9%, p=0.001).This retrospective study suggests that combination therapy with lidocaine and amiodarone can terminate most refractory ventricular arrhythmias. Even in patients with a sufficient LVEF not receiving amiodarone, it is possible that lidocaine can contribute to a favorable outcome.
- Decreased IK1 and increased ryanodine receptor sensitivity synergistically contribute to sustained focal arrhythmia in the intact rabbit heart. [JOURNAL ARTICLE]
- J Physiol 2014 Sep 5.
Heart failure (HF) results in dramatic electrophysiological remodeling, including increased sensitivity of ryanodine receptors (RyR) and decreased inward rectifying K(+) current (IK1), which predisposes HF myocytes to delayed afterdepolarizations and triggered activity. Therefore, we sought to determine the role of increased RyR sensitivity and decreased IK1 in contributing to focal arrhythmia in the intact non-failing heart. Optical mapping of transmembrane potential and intracellular Ca(2+) was performed in Langendorff-perfused rabbit hearts (n = 15). Local β-adrenergic receptor stimulation with norepinephrine (NE, 50μL, 250μM) was applied to elicit focal activity (premature ventricular complexes [PVCs] or ventricular tachycardia [VT≥3 beats]). NE was administered under control conditions (CTL) and following pretreatment with 50μM BaCl2 to reduce IK1, or 200μM caffeine (Caff) to sensitize RyR, both alone and in combination. Local NE injection resulted in Ca(2+)-driven PVCs arising from the injection site in all hearts studied. No increase in NE-mediated PVCs was observed following pretreatment with either BaCl2 or Caff alone (CTL: 1.1±0.7, BaCl2: 1.0±0.7, Caff: 1.3±0.8 PVCs/injection, p = NS). However, pretreatment with the combination of BaCl2+Caff resulted in a significant increase in PVCs (2.3±2.8 PVCs/injection, p<0.05 vs. CTL, BaCl2, Caff). Additionally, pretreatment with BaCl2+Caff lead to sustained monomorphic VT arising from the NE application site in all hearts studied, which lasted up to 6min following a single NE injection. VT was never observed under any other condition, suggesting synergism between increased RyR sensitivity and decreased IK1 in contributing to focal activity. These findings may have important implications for the understanding and prevention of focal arrhythmia in HF. (250) This article is protected by copyright. All rights reserved.
- Structure Driven Design of Novel Human Ether-A-Go-Go-Related-Gene Channel (hERG1) Activators. [Journal Article]
- PLoS One 2014; 9(9):e105553.
One of the main culprits in modern drug discovery is apparent cardiotoxicity of many lead-candidates via inadvertent pharmacologic blockade of K+, Ca2+ and Na+ currents. Many drugs inadvertently block hERG1 leading to an acquired form of the Long QT syndrome and potentially lethal polymorphic ventricular tachycardia. An emerging strategy is to rely on interventions with a drug that may proactively activate hERG1 channels reducing cardiovascular risks. Small molecules-activators have a great potential for co-therapies where the risk of hERG-related QT prolongation is significant and rehabilitation of the drug is impractical. Although a number of hERG1 activators have been identified in the last decade, their binding sites, functional moieties responsible for channel activation and thus mechanism of action, have yet to be established. Here, we present a proof-of-principle study that combines de-novo drug design, molecular modeling, chemical synthesis with whole cell electrophysiology and Action Potential (AP) recordings in fetal mouse ventricular myocytes to establish basic chemical principles required for efficient activator of hERG1 channel. In order to minimize the likelihood that these molecules would also block the hERG1 channel they were computationally engineered to minimize interactions with known intra-cavitary drug binding sites. The combination of experimental and theoretical studies led to identification of functional elements (functional groups, flexibility) underlying efficiency of hERG1 activators targeting binding pocket located in the S4-S5 linker, as well as identified potential side-effects in this promising line of drugs, which was associated with multi-channel targeting of the developed drugs.
- Left ventricular noncompaction - a case report. [Journal Article]
- Mymensingh Med J 2014 Jul; 23(3):581-5.
Left Ventricular (LV) noncompaction is a rare disorder of endomyocardial morphogenesis. It has got a high mortality rate. It is frequently missed during diagnosis because of lack of suspicion and lack of definite diagnostic criteria. We are reporting a case of LV noncompaction in a Bangladeshi patient. Patient presented to us with history of repeated syncope. She had family history of sudden cardiac death. Clinically, there had a systolic murmur in left parasternal area. Her ECG showed different arrhythmia like atrial fibrillation, sinus bradycardia and Ventricular tachycardia. Her echocardiography showed features consistent with 'left ventricular noncompaction'. This is the first case report of this type in a Bangladeshi patient.
- Tachycardia-induced cardiomyopathy. [Journal Article]
- ARYA Atheroscler 2014 May; 10(3):175-8.
Tachycardia-induced cardiomyopathy (TIC) is a rare cause of dilated cardiomyopathy (DCMP). The diagnosis can be missed because tachycardia is a common symptom in DCMP.We reviewed a case 5-year-old with palpitation and dyspnea with symptoms and signs of heart failure that diagnosed as DCMP initially. Then, in the evaluation for cause of tachycardia, atrial tachycardia was detected. Hence, treatment with flecainide was started and after 3 months, left ventricular (LV) systolic function and symptoms of the patient was relieved.TIC should be suspected in all patients with unexplained LV dysfunctions in the setting of a persistent tachyarrhythmia.
- Quantifying late gadolinium enhancement on CMR provides additional prognostic information in early risk-stratification of nonischemic cardiomyopathy: a cohort study. [JOURNAL ARTICLE]
- BMC Cardiovasc Disord 2014 Aug 27; 14(1):110.
Suspected nonischemic cardiomyopathy (NICM) is a common clinical setting with highly variable prognosis. Early noninvasive risk-stratification is important for justification of invasive examinations, specific treatment and patient surveillance. We studied the additional prognostic value of late gadolinium enhancement (LGE) and segmental wall motion abnormality (SWMA) extent on cardiovascular magnetic resonance (CMR) compared to traditional risk factors in suspected NICM.In this observational cohort study, we enrolled 86 consecutive patients referred for CMR due to suspected NICM. Patients with ischemic cardiomyopathy were excluded. CMR images were analysed for left ventricular LGE and SWMA extents and patients were followed-up for major adverse cardiac events (MACE), including cardiovascular death, aborted sudden death and cardiac transplantation.Of 86 patients (median age: 53 years, 45% female), mainly presenting with ventricular arrhythmias (40%) and congestive heart failure (44%), 76% were finally diagnosed with NICM, 17% with left ventricle hypertrophy and 7% with idiopathic arrhythmia. On CMR, 61 patients (71%) had LGE and 56 (65%) SWMA. During median follow-up of 835 days, 15 patients (17%) reached MACE. In univariant analysis, LGE volume (hazard ratio [HR] 1.028 per 1% increase in LGE, p < 0.001), left ventricular ejection fraction (LVEF) (HR 0.959, p = 0.009) and SWMA score (HR 1.067, p = 0.012) had strongest associations with MACE. In multivariate analysis, the best overall model for event prediction included LGE volume (HR 1.027, p = 0.003), sustained ventricular tachycardia (HR 4.7, p = 0.011) and LVEF (HR 0.962, p = 0.034). Among patients with LGE, there was an event rate of 26% (14 of 61) versus 4% (1 of 25) in patients without LGE (p = 0.041, Log-rank). The highest event rate was observed in patients with LGE volume of >=17%. Patients without SWMA did not experience MACE (p = 0.002, Log-rank), giving additional information in the subgroup of patients with preserved LVEF (>=50%).In suspected NICM, presenting with ventricular arrhythmias or heart failure, LGE extent gives additional prognostic information compared to traditional risk factors, while the absence of SWMA may give prognostic information beyond normal LVEF. Even though the final diagnosis is uncertain in NICM, extensive amount of LGE should be considered as a sign of poor prognosis.
- Relation of Strain by Feature Tracking and Clinical Outcome in Children, Adolescents, and Young Adults With Hypertrophic Cardiomyopathy. [JOURNAL ARTICLE]
- Am J Cardiol 2014 Jul 30.
Evaluation of hypertrophic cardiomyopathy (HC) in young patients is limited by lack of age-specific norms for wall thickness on cardiovascular magnetic resonance (CMR) images. Left ventricular strain may have a role in identifying and risk stratifying patients with HC, but few data exist for strain measurement on CMR images. In 30 patients (14.1 ± 3.2 years) with clinically diagnosed HC and 24 controls (15.6 ± 2.8 years), strain (radial, longitudinal, and circumferential) was evaluated by 2 experienced readers using CMR feature tracking. In patients with HC, hypertrophied segments had decreased radial (28.0 ± 5.2% vs 58.6 ± 3.9%, p = 0.0002), circumferential (-23.7 ± 1.1% vs -28.3 ± 0.8%, p = 0.004), and longitudinal (-11.2 ± 1.2% vs -21.7 ± 0.8%, p <0.0001) strains versus control segments. Hypertrophied segments had decreased longitudinal (basal segments -12.2 ± 1.9% vs -22.6 ± 1.2%, p = 0.0002), radial (basal segments 22.7 ± 10.8% vs 78.8 ± 7.2%, p = 0.0001), and circumferential (basal segments -22.4 ± 1.7% vs -30.6 ± 1%, p = 0.0004) strains versus nonhypertrophied segments in patients with HC. Longitudinal strain had the lowest intraobserver and interobserver variabilities (coefficient of variability -15.7% and -18.5%). After a median follow-up of 28.1 months (interquartile range [IQR] 4.2 to 33.1), 7 patients with HC with an adverse event outcome (5 ventricular tachycardia, 1 appropriate implantable cardioverter-defibrillator discharge, and 1 death) had reduced global radial (median 39.7%, IQR 39.6% to 46.6% vs 65.4%, IQR 46.1% to 83.4%, p = 0.01) and longitudinal strains (median -16.5%, IQR -18.7% to -15.5% vs -19.7%, IQR -23.8% to -17.5%, p = 0.046) compared with patients with HC without an event. In conclusion, CMR feature tracking detects differences in global and segmental strains and may represent a novel method to predict clinical outcome in patients with HC. Further study is necessary to evaluate longitudinal changes in this population.
- Catheter ablation of ventricular tachycardia beneath an endoventricular patch. [Journal Article]
- Circulation 2014 Aug 26; 130(9):801-2.
- Exogenous midkine administration prevents cardiac remodeling in pacing-induced congestive heart failure of rabbits. [JOURNAL ARTICLE]
- Heart Vessels 2014 Aug 26.
Midkine (MK), a heparin-binding growth factor, has been shown to prevent cardiac remodeling after ischemic injury through its anti-apoptotic effect. Cell apoptosis is central to the pathophysiology of cardiac remodeling in congestive heart failure (CHF) of ischemic as well as non-ischemic origin. We hypothesized that MK exerts the anti-apoptotic cardioprotective effect in CHF of non-ischemic etiology. MK protein or vehicle (normal saline) was subcutaneously administered in tachycardia-induced CHF rabbits (right ventricular pacing, 350 beats/min, 4 weeks). The vehicle-treated rabbits (n = 19, control) demonstrated severe CHF and high mortality rate, whereas MK (n = 16) demonstrated a well-compensated state and a lower mortality rate. In echocardiography, left ventricular (LV) end-diastolic dimension decreased in MK versus control, whereas LV systolic function increased. In histological analysis (picrosirius red staining), MK decreased collagen deposition area compared with control. TUNEL staining showed that MK prevented cell apoptosis and minimized myocyte loss in the CHF rabbit ventricle, associated with activation of PI3-K/Akt signaling, producing a parallel decrease of Bax/Bcl-2 ratio. MK prevented progression of cardiac remodeling in the CHF rabbit, likely by activation of anti-apoptotic signaling. Exogenous MK application might be a novel therapeutic strategy for CHF due to non-ischemic origin.