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Biomedical subjects

E Kevin Heist

Publications and source records attributed to E Kevin Heist.

16 recordsLinked to original sources
PubMed2006

Left ventricular lead electrical delay predicts response to cardiac resynchronization therapy.

BACKGROUND: Intracardiac electrograms can be used to guide left ventricular (LV) lead placement during implantation of cardiac resynchronization therapy (CRT) devices. Although attempts often are made to ensure that the LV lead is positioned at a site of maximal electrical delay, information on whether this is useful in predicting the acute hemodynamic response and long-term clinical outcome to CRT is limited. OBJECTIVES: The purpose of this study was to assess the ability of intracardiac (electrogram) measurements made during LV lead placement in patients undergoing CRT for predicting acute hemodynamic response and long-term clinical outcome to CRT. METHODS: Seventy-one subjects with standard indications for CRT underwent electrogram measurements and echocardiograms performed in the acute phase of this study. The LV lead electrical delay was measured intraoperatively from the onset of the surface ECG QRS complex to the onset of the sensed electrogram on the LV lead, as a percentage of the baseline QRS interval. Echocardiographic assessment of the hemodynamic response to CRT was measured as an intra-individual percentage change in dP/dt over baseline (DeltadP/dt, derived from the mitral regurgitation Doppler profile) with CRT on and off. dP/dt was measurable in 48 subjects, and acute responders to CRT were defined as those with DeltadP/dt >or=25%. Long-term response was measured as a combined endpoint of hospitalization for heart failure and/or all cause mortality at 12 months. Time to the primary endpoint was estimated by the Kaplan-Meier method, with comparisons made using the log rank test. RESULTS: LV lead electrical delay correlated weakly with DeltadP/dt of the combined group (n = 48, r = 0.311, P = .029) but was strongly correlated with DeltadP/dt in the nonischemic subgroup (n = 20, r = 0.48, P = .027). LV lead electrical delay (%) was significantly longer in acute responders (69.6 +/- 23.9 vs 31.95 +/- 11.57, P = .002) among patients with nonischemic cardiomyopathy. A reduced LV lead electrical delay (<50% of the QRS duration) was associated with worse clinical outcome within the entire cohort (hazard ratio: 2.7, 95% confidence interval: 1.17-6.68, P = .032) as well as when stratified into ischemic and nonischemic subgroups. CONCLUSION: Measuring LV lead electrical delay is useful during CRT device implantation because it may help predict hemodynamic response and long-term clinical outcome.

Aged↗
PubMed2006

Analysis of the left atrial appendage by magnetic resonance angiography in patients with atrial fibrillation.

BACKGROUND: Recent interest has focused on the left atrial appendage (LAA) in the setting of atrial fibrillation as a potential source of thromboembolism and stroke, which may be amenable to permanent occlusion by a variety of investigational catheter-delivered devices. Precise anatomic characterization of the LAA is necessary to determine the suitability of a patient for device placement and for device selection and sizing. OBJECTIVES: The purpose of this study was to perform detailed three-dimensional characterization of LAA size and geometry by magnetic resonance angiography. METHODS: Fifty patients with chronic atrial fibrillation undergoing cardiac magnetic resonance angiography in preparation for catheter ablation of atrial fibrillation were analyzed for LAA volume, neck size, depth, and overall geometry. RESULTS: The average LAA volume was 17.3 +/- 6.7 mL, with a depth of 26.6 +/- 4.9 mm and a "neck" diameter of 20.0 +/- 5.3 mm x 14.1 +/- 4.7 mm. The average number of LAA lobes was 1.4 +/- 0.7 (range 1-4). Substantial interpatient variability was present in the relative dimensions and morphology of the LAA. There was a significant correlation between left atrial size and LAA neck dimensions. CONCLUSION: There is significant heterogeneity in LAA size and dimensions among patients with atrial fibrillation. Device occlusion of the LAA may require devices that are available in multiple sizes/shapes or that can adapt to this heterogeneity.

Atrial Appendage↗
PubMed2006

Usefulness of a novel "response score" to predict hemodynamic and clinical outcome from cardiac resynchronization therapy.

Cardiac resynchronization therapy (CRT) is an important treatment for patients with congestive heart failure and ventricular dyssynchrony, but response to CRT is highly variable. We assessed whether a scoring system that encompasses a combination of patient selection and procedural variables would improve prediction of CRT response. Thirty-nine patients who underwent CRT with echocardiographic assessment of baseline contractility and left ventricular (LV) dyssynchrony, intraprocedural assessment of LV lead electrical delay, and postprocedural chest radiography were included. Baseline LV dyssynchrony was measured by Doppler tissue velocity imaging as the maximum time difference between peak systolic velocity of anterior, lateral, posterior, and septal walls. The hemodynamic effect of CRT was measured by Doppler analysis of mitral regurgitation as percent change in maximal +dP/dt (DeltadP/dt) with CRT on versus off. Acute responders to CRT were defined as Deltadp/dt >or=25%. Clinical response was measured as a combined end point of hospitalization for heart failure and all-cause mortality. A 4-point response score was generated using variables associated with DeltadP/dt and assigning 1 point for a dorsoventral LV/right ventricular interlead distance>10 cm, 1 point for a LV lead electrical delay>or=50%, 1 point for a baseline maximum +dP/dt <600 mm Hg/s, and 1 point for a maximum time difference>100 ms. In conclusion, there was a significant association between response score (0 to 4 points) and acute hemodynamic response to CRT (p<0.0001). Kaplan-Meier analysis associated a higher response score with improved 12-month event-free survival after CRT implantation (p=0.0019).

Aged↗
PubMed2006

Left ventricular lead proximity to an akinetic segment and impact on outcome of cardiac resynchronization therapy.

BACKGROUND: Previous studies report that the optimal pacing site for cardiac resynchronization therapy (CRT) is along the left ventricular (LV) lateral and postero-lateral (PL) wall. However, little is known regarding whether pacing over an akinetic site impacts the contractile response and long-term outcome from CRT. METHODS AND RESULTS: A total of 38 patients with ischemic cardiomyopathy were studied for their acute hemodynamic and 12-month clinical response to CRT. The intraindividual percentage change in dP/dt (%DeltadP/dt), over baseline, was derived from the mitral regurgitation (MR) Doppler profile with CRT on versus off. Two-dimensional echocardiography was used for myocardial segmentation and determinination of akinetic sites. LV lead implant site was determined using angiographic and radiographic data and categorized as being "on" (group 1) or "off" (group 2) an akinetic site. Long-term response was measured as a combined endpoint of hospitalization for heart failure and/or all cause mortality at 12 months. Time to primary endpoint was estimated by the Kaplan-Meier method. Clinical characteristics and acute hemodynamic response was similar in both (group 1 [n = 14]; %DeltadP/dt 48.8 +/- 67.4% vs group 2 [n = 24]; %DeltadP/dt 32.2 +/- 40.1%, P = 0.92). No difference in long-term outcome was observed (P = 0.59). In contrast, lead placement in PL or mid-lateral (ML) positions was associated with a better acute hemodynamic response when compared to antero-lateral (AL) positions (PL, %DeltadP/dt 45.7 +/- 50.7% and ML, %DeltadP/dt 45.1 +/- 58.8% vs AL, %DeltadP/dt 2.9 +/- 30.9%, respectively, P = 0.014). CONCLUSION: LV lead proximity to an akinetic segment does not impact acute hemodynamic or 12-month clinical response to CRT.

Aged↗
PubMed2005

Radiographic left ventricular-right ventricular interlead distance predicts the acute hemodynamic response to cardiac resynchronization therapy.

Placement of left ventricular (LV) and right ventricular (RV) leads with maximal interlead separation is frequently sought during cardiac resynchronization therapy (CRT), but few published data are available to support this. This study examined the relation between LV and RV lead separation and the acute effects of CRT on cardiac contractility. A total of 51 consecutive patients who underwent CRT for standard indications with sufficient mitral regurgitation for echocardiographic assessment of contractility (using Doppler profiles of mitral regurgitation as a percentage of change in dP/dt [DeltadP/dt] with CRT on and off), successful transvenous LV lead placement, and postprocedural chest radiography were evaluated. The separation of the LV and RV lead tips (direct interlead distance and horizontal and vertical components) was determined on postprocedural posteroanterior and lateral radiographs. The corrected direct LV-RV interlead distance on the lateral radiograph was correlated with the DeltadP/dt (n = 51, r = 0.43, p = 0.002). The lateral interlead distance in the horizontal plane (r = 0.58, p <0.0001), but not the vertical plane (r = -0.28, p = NS), correlated with the DeltadP/dt. The corrected horizontal interlead distance on the lateral film was greater in acute hemodynamic responders to CRT (DeltadP/dt >25%) compared with nonresponders (14.4 +/- 5.4 vs 9.2 +/- 5.8 cm, p = 0.002). Other LV-RV measures on the posteroanterior and lateral radiographs did not correlate with the DeltadP/dt. Use of these findings may help to guide the sites of LV and RV lead placement to maximize the benefit derived from CRT.

Aged↗
PubMed2005

The coronary venous anatomy: a segmental approach to aid cardiac resynchronization therapy.

The coronary sinus is the gateway for left ventricular (LV) epicardial lead placement for cardiac resynchronization therapy. The implanting electrophysiologist is usually challenged by a high degree of variability in the coronary venous anatomy, making it important to have a more consistent and uniform segmental approach to describe the coronary venous tree and its branches. Classifying the coronary sinus branches and tributaries by the segment of their location rather than by conventional anatomic names (i.e., middle cardiac vein, great cardiac vein, and so on), would provide more relevant anatomic and functional information at the time of LV lead placement. This would enable the implanting physician to proactively correlate the venous anatomy with the segmental wall motion abnormalities or dyssynchrony, as defined by echocardiography and other imaging modalities. The current viewpoint calls for a more systematic segmental approach for describing the coronary venous anatomy.

Cardiac Pacing, Artificial↗
PubMed2005

Enhancement of cardiac function and suppression of heart failure progression by inhibition of protein phosphatase 1.

Abnormal calcium cycling, characteristic of experimental and human heart failure, is associated with impaired sarcoplasmic reticulum calcium uptake activity. This reflects decreases in the cAMP-pathway signaling and increases in type 1 phosphatase activity. The increased protein phosphatase 1 activity is partially due to dephosphorylation and inactivation of its inhibitor-1, promoting dephosphorylation of phospholamban and inhibition of the sarcoplasmic reticulum calcium-pump. Indeed, cardiac-specific expression of a constitutively active inhibitor-1 results in selective enhancement of phospholamban phosphorylation and augmented cardiac contractility at the cellular and intact animal levels. Furthermore, the beta-adrenergic response is enhanced in the transgenic hearts compared with wild types. On aortic constriction, the hypercontractile cardiac function is maintained, hypertrophy is attenuated and there is no decompensation in the transgenics compared with wild-type controls. Notably, acute adenoviral gene delivery of the active inhibitor-1, completely restores function and partially reverses remodeling, including normalization of the hyperactivated p38, in the setting of pre-existing heart failure. Thus, the inhibitor 1 of the type 1 phosphatase may represent an attractive new therapeutic target.

Animals↗
PubMed2005

Drug-induced proarrhythmia and use of QTc-prolonging agents: clues for clinicians.

Use of drugs with the potential for prolongation of the QTc interval and proarrhythmia is a growing challenge facing clinicians. Many pharmaceutical agents have been denied approval for human use, approved with restrictions and warnings regarding proarrhythmia, or withdrawn from the market based upon arrhythmic risk. Despite known risk factors for QTc prolongation and drug-induced arrhythmia, precise prediction of the risk of torsades de pointes (TdP) in an individual patient remains difficult. The mechanism of drug-induced TdP typically involves use of an agent that blocks the I(Kr) cardiac potassium current, often in combination with risk-amplifying factors such as high drug levels, reduced drug metabolism, polypharmacy, and patient-specific factors such as gender, age, and genetic polymorphism. For the clinician, an integrated approach involving appreciation of the risk factors for proarrhythmia combined with computer-based risk assessment is the best method for reducing the risk of drug-induced proarrhythmia in clinical practice.

Anti-Arrhythmia Agents↗
PubMed2005

Treating atrial fibrillation. What is the consensus now?

Atrial fibrillation (AF) is a common cardiac arrhythmia, especially in elderly persons. Current recommendations outline pharmacologic and interventional therapies designed to minimize the risk of stroke and other morbidities that can accompany this condition. In this article, Drs Basu Ray and Heist review treatment options for cardioversion and control of rate and rhythm and make suggestions for best management in patients with chronic or intermittent AF.

Anti-Arrhythmia Agents↗
PubMed2004

Catheter ablation of atrial flutter after orthotopic heart transplantation.

INTRODUCTION: Atrial arrhythmias, including atrial flutter, are common in orthotopic heart transplant recipients. However, only a small number of individual case reports describe the electrical circuit and catheter ablation of atrial flutter after heart transplantation. METHODS AND RESULTS: Detailed electrophysiologic evaluation and radiofrequency ablation of atrial flutter were performed in three patients after orthotopic heart transplantation. All cases involved a counterclockwise flutter circuit around the tricuspid annulus. All were successfully ablated at the isthmus between the tricuspid valve and the atrial anastomosis adjacent to the inferior vena cava. CONCLUSION: Atrial flutter involving a counterclockwise circuit around the tricuspid annulus is common in the heart transplant population. Based on the patients described in this study and other cases reported in the literature, this arrhythmia often is treated successfully by ablation of the isthmus between the tricuspid valve and the atrial anastomosis near the inferior vena cava.

Adult↗
PubMed2003

Telomerase and the aging heart.

Telomeres are highly conserved structures that cap and protect the ends of linear chromosomes. The telomerase enzyme is present in germline cells as well as in many rapidly dividing tissues and serves to maintain chromosome length and integrity during cell division. Telomerase activity is typically reduced as an organism ages, and this phenomenon has been implicated in the aging process. In this Perspective, we focus on the effects of both gene knockout and gene replacement of telomerase in the heart and discuss the implications of these findings for potential cardiovascular therapeutics.

Aging↗
PubMed2003

Apoptosis in heart failure and the senescent heart.

The progressive loss of cardiac myocytes by apoptotic cell death has been discussed as an important pathogenic component in the failing myocardium as well in the aging heart. The degree to which apoptosis contributes to myocyte loss in these conditions, however, is a controversial issue. This review focuses on the regulation of apoptosis, evidence implicating apoptosis as a mechanism for the progression and development of heart failure, the role of apoptotic death in senescent cardiac dysfunction, as well as on the problems of detection of apoptosis.

Aging↗
PubMed2002

Titin--springing back to youth?

Mutations in the muscle protein titin have been linked to dilated cardiomyopathy, a condition in which the heart chambers are enlarged and blood is ineffectively pumped, in humans and in animal models. This protein, which is a component of sarcomeres, provides essential scaffolding for other muscle proteins and acts as a spring to confer passive elasticity on the cardiomyocyte. Several titin isoforms exist, and they display varying size and degrees of elasticity. We review two interesting reports that show how variations in titin isoforms might be implicated in cardiac failure.

Aging↗
PubMed2002

Protein kinase A negatively modulates the nuclear accumulation of NF-ATc1 by priming for subsequent phosphorylation by glycogen synthase kinase-3.

The nuclear localization and transcriptional activity of the NF-ATc family of transcription factors, essential to many developmental, differentiation, and adaptation processes, are determined by the opposing activities of the phosphatase calcineurin, which promotes nuclear accumulation of NF-ATc, and several kinases, which promote cytoplasmic accumulation. Many reports suggest that protein kinase A (PKA) negatively modulates calcineurin-mediated NF-ATc activation. Here we show that overexpression of PKA causes phosphorylation and cytoplasmic accumulation of NF-ATc1 in direct opposition to calcineurin by phosphorylating Ser-245, Ser-269, and Ser-294 in the conserved serine-proline repeat domain, and that mutation of these serines blocks the effect of PKA. Activation of endogenous PKA is similarly able to promote phosphorylation of these sites on NF-ATc1 in two lymphoid cell lines. We further show that a complete block of NF-ATc1 nuclear localization by PKA requires a second kinase activity that can be supplied by glycogen synthase kinase-3 (GSK-3), and that mutation of either the PKA phosphorylation sites or the upstream GSK-3 sites prevents the effect of PKA. Thus, we propose that PKA functions cooperatively as a priming kinase for further phosphorylation by GSK-3 to oppose calcineurin-mediated nuclear accumulation and transcriptional activity of NF-ATc1 and that, through this mechanism, PKA may be an important modulator of many NF-ATc-dependent processes.

Amino Acid Sequence↗
PubMedDate not supplied

Atrial fibrillation and congestive heart failure: risk factors, mechanisms, and treatment.

Atrial fibrillation (AF) and congestive heart failure (CHF) are commonly encountered together, and either condition predisposes to the other. Risk factors for AF and CHF include age, hypertension, valve disease, and myocardial infarction, as well as a variety of medical conditions and genetic variants. Congestive heart failure and AF share common mechanisms, including myocardial fibrosis and dysregulation of intracellular calcium and neuroendocrine function. Pharmacological treatments including beta-blockers, digoxin, angiotensin-converting enzyme inhibitors and angiotensin receptor blockers can be useful in treating both of these conditions. Antiarrhythmic medications intended to achieve and maintain sinus rhythm may be beneficial in some patients with AF and CHF. Advances in pacemaker and defibrillator therapy, including cardiac resynchronization therapy, may also benefit patients with AF and CHF. Surgical and catheter-based ablation therapy can restore sinus rhythm in patients with AF, with proven benefit in patients with concommitant CHF. Investigational biologic therapy, including cell and gene based therapy, offers promise for the future of reversing the pathophysiological mechanisms that underlie AF and CHF.

Atrial Fibrillation↗