Tachycardia Induced Cardiomyopathy

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Francis G Spinale - One of the best experts on this subject based on the ideXlab platform.

  • cellular and extracellular remodeling with the development and recovery from Tachycardia Induced Cardiomyopathy changes in fibrillar collagen myocyte adhesion capacity and proteoglycans
    Journal of Molecular and Cellular Cardiology, 1996
    Co-Authors: Francis G Spinale, James L Zellner, Wendy S Johnson, D M Eble, Paul D Munyer

    The myocardial extracellular matrix (ECM) is composed of three important constituents: (1) fibrillar collagen, (2) a basement membrane, and (3) proteoglycans. Structural or compositional changes in these ECM components may affect left ventricular (LV) function as well as influence overall LV geometry. Accordingly, this study examined the relationship between changes in these ECM components to changes in LV function and geometry which develop with the progression and regression from supraventricular Tachycardia-Induced Cardiomyopathy (SVT). LV function and specific components of the ECM were studied in pigs with SVT Cardiomyopathy (SVT:atrially paced 240 bpm, 3 weeks; n = 7), or after a 4-week recovery from SVT Cardiomyopathy (post-SVT; n = 6), and in controls (n = 7). LV fractional shortening fell by 60% and end-diastolic dimension increased by 47% with SVT compared to controls. While LV fractional shortening normalized with post-SVT, end-diastolic dimension remained 40% higher than controls. Collagen concentration fell by 22% and salt extractable collagen, which reflects collagen cross-linking, increased by 41% with SVT compared to controls. Collagen concentration increased by 20%, collagen extraction normalized, and levels of collagen type III mRNA increased by 42% with post-SVT. Isolated myocyte adhesion capacity to basement membrane substrates laminin, fibronectin, and collagen type IV were examined. SVT resulted in over a 50% reduction in myocyte adhesion for all of the basement membrane components compared to controls. A normalization in isolated myocyte adhesion capacity was observed in post-SVT. The relative content and distribution of the ECM proteoglycan chondroitin sulfate was examined using immunohistochemistry. With SVT, the density of this proteoglycan increased around individual myocytes. With post-SVT, the relative distribution of chondroitin sulfate returned to control levels. Thus, SVT Cardiomyopathy was associated with reduced collagen concentration and cross-linking, diminished myocyte basement membrane adhesion capacity, and increased proteoglycans. Recovery from SVT Cardiomyopathy resulted in increased collagen concentration, and a normalization of myocyte adhesion capacity and proteoglycan distribution. These results suggest that changes within the ECM are a dynamic process and accompany the LV systolic and diastolic function as well as ventricular and myocyte remodeling during the progression and regression from cardiomyopathic disease.

  • myocyte electrophysiological properties following the development of supraventricular Tachycardia Induced Cardiomyopathy
    Journal of Molecular and Cellular Cardiology, 1995
    Co-Authors: Rupak Mukherjee, Kenneth W Hewett, Francis G Spinale

    Chronic supraventricular Tachycardia (SVT) causes left ventricular (LV) dilatation and dysfunction, diminished myocyte contractile function, and abnormalities in sarcolemmal receptor systems. We hypothesized that changes in myocyte action potential characteristics and l -type Ca 2+ channel (Ca 2+ channel) function, which are major determinants of myocyte contractile processes, would occur with SVT Cardiomyopathy. LV function and isolated myocyte contractile function were examined in 11 pigs with SVT Cardiomyopathy (pace 240 bpm; 3 weeks) and 11 control pigs. With chronic SVT. LV fractional shortening fell and myocyte shortening velocity was reduced compared to controls (11 ± 2 v 37 ± 2%. P v 55.7 ± 1.6 μ m/s. P v 129.5 ± 3.1 V/s, P v 110.3 ± 1.3 mV, P v 169.1 ± 6.8 ms, P =0.002). These specific abnormalities in the indices of myocyte contractile function and action potential characteristics which occurred with SVT Cardiomyopathy were not normalized following β -adrenergic receptor stimulation. In order to determine a potential mechanism for the changes in myocyte contractile function and action potential characteristics with SVT Cardiomyopathy, Ca 2+ channel function was examined in control and SVT myocytes. In SVT myocytes, peak l -type Ca 2+ current (I Ca ) normalized to membrane capacitance and the Ca 2+ channel inactivation time constant were reduced compared to controls (−2.30 ± 0.24 v −3.79 ± 0.28 pA/pF, P = 0.0001; and 104.0 ± 10.8 v 199.9 ± 27.4 ms, P = 0.005, respectively). The abnormalities in Ca 2+ channel function with SVT Cardiomyopathy persisted in myocytes with equivalent membrane capacitances and were not normalized with β -adrenergic receptor stimulation. In conclusion, findings from the present study suggest that fundamental abnormalities in myocyte electrical events (action potential) and ionic flux (Ca 2+ channel function) are contributory mechanisms for the depressed myocyte contractile function with SVT Cardiomyopathy.

  • lv and myocyte structure and function after early recovery from Tachycardia Induced Cardiomyopathy
    American Journal of Physiology-heart and Circulatory Physiology, 1995
    Co-Authors: Francis G Spinale, Rupak Mukherjee, Henry H Holzgrefe, S R Arthur, M J Child, James R Powell, William H Koster

    Left ventricular (LV) function and mass were measured in six conscious dogs at weekly intervals during the progression of Tachycardia-Induced dilated Cardiomyopathy (DCM) and during a 1-mo recovery period from DCM (post-DCM). LV end-diastolic volume and LV wall stress increased and LV ejection fraction decreased with each week of pacing. Despite the increased LV wall stress, LV mass did not change during the progression of Tachycardia DCM. One week post-DCM resulted in an improved LV ejection fraction and normalization of neurohormonal profiles. However, 1 wk post-DCM was accompanied by a 26% increase in LV mass and persistent LV chamber dilation. Isolated myocyte function was examined and compared with that in six normal control dogs. Myocyte percent and myocyte velocity of shortening were 19 and 32% lower, respectively, in the post-DCM group compared with controls. Thus termination of the Tachycardia subsequent to the development of DCM resulted in persistent LV chamber dilation and abnormalities in myocyte contractile function. The improved LV pump function with early recovery from Tachycardia-Induced DCM was mediated by LV hypertrophy and a subsequent reduction in LV wall stress rather than a normalization of LV geometry and myocyte contractile function.

  • the cellular basis for the blunted response to beta adrenergic stimulation in supraventricular Tachycardia Induced Cardiomyopathy
    Journal of Molecular and Cellular Cardiology, 1993
    Co-Authors: Ryuhei Tanaka, B M Fulbright, Rupak Mukherjee, S A Burchell, Fred A Crawford, Michael R Zile, Francis G Spinale

    Chronic Tachycardia-Induced dilated Cardiomyopathy causes increased plasma catecholamines and alterations in beta-adrenergic responsiveness in vivo. However, whether isolated myocyte contractile response to beta-stimulation is directly affected by the development of Cardiomyopathy and how these changes are related to alterations in the beta-adrenergic receptor system remain unclear. Accordingly, isolated myocyte function and beta-adrenergic responsiveness were examined in two groups of 12 pigs each: sham controls, and with supraventricular Tachycardia Induced Cardiomyopathy (SVT; pace: 240 beats/min, 3 weeks). Isolated LV myocyte percent and velocity of shortening were examined at baseline, with isoproterenol (2-100 nM), and forskolin (0.1-4 microM). Baseline percent and velocity of shortening were significantly reduced with SVT compared to controls (1.6 +/- 0.1 vs 5.4 +/- 0.2%, 56 +/- 3 vs 25 +/- 1 micron/s, respectively, P < 0.05). The maximal increase in the percent and velocity of shortening with isoproterenol was significantly blunted in the SVT myocytes compared with controls (3.2 +/- 0.4 vs 9.7 +/- 1.0%, 48.0 +/- 5.3 vs 122.6 +/- 15.5 micron/s, respectively, P < 0.05). Similarly, maximal increase in the percent and velocity of shortening with forskolin were reduced with SVT compared to controls (3.3 +/- 0.4 vs 10.5 +/- 0.6%, 50.7 +/- 6.4 vs 120.1 +/- 9.7 micron/s, respectively, P < 0.05). In order to determine the cellular basis for these changes in beta-adrenergic response, myocyte structure, sarcolemmal beta-receptor density and affinity, and adenylate cyclase activity were examined. There was a 25% reduction in beta-receptor number with SVT (P < 0.05) but no change in affinity. Basal adenylate cyclase activity was lower with SVT compared to control (46 +/- 3 vs 77 +/- 10 pmol cyclic AMP/mg/min, P < 0.05), and exhibited a blunted response with both isoproterenol (1 mM; 106 +/- 19 vs 203 +/- 26 pmol cyclic AMP/mg/min, P < 0.05) and forskolin (100 microns: 209 +/- 35 vs 378 +/- 58 pmol cyclic AMP/mg/min, P < 0.05). Finally, myofibrillar content within SVT myocytes was significantly reduced from controls (43 +/- 7 vs 63 +/- 4%, P < 0.05). In summary, the cellular basis for the depressed myocyte contractile response to beta-stimulation with Tachycardia Induced SVT are probably due to several factors which include: decreased expression of beta-receptors, alterations in beta-receptor transduction, reduced adenylate cyclase activity, and decreased myocyte contractile protein content.

  • relation between ventricular and myocyte function with Tachycardia Induced Cardiomyopathy
    Circulation Research, 1992
    Co-Authors: Francis G Spinale, B M Fulbright, Rupak Mukherjee, Fred A Crawford, R Tanaka, Michael R Zile

    Chronic supraventricular Tachycardia (SVT) causes left ventricular (LV) dilatation and dysfunction. Changes in myocyte function and structure may be important factors in the development of SVT Cardiomyopathy. Accordingly, LV function and isolated myocyte structure and function were examined in six pigs with pacing-Induced SVT Cardiomyopathy (3 weeks at 240 beats per minute) and six control pigs. LV function was examined by simultaneous echocardiography and catheterization, and isolated myocyte function was studied using computer-assisted video microscopy. Indexes of isolated myocyte contractile performance were examined in the unloaded, unattached state (31 control and 24 SVT cells) and after attachment to a basement membrane substrate (65 control and 45 SVT cells). LV fractional shortening and peak +dP/dt significantly decreased in SVT cells compared with control cells (12 +/- 2% versus 28 +/- 2%, and 842 +/- 61 versus 1,216 +/- 119 mm Hg/sec, respectively; p less than 0.05). Isolated myocyte percent shortening and normalized peak velocity of shortening of SVT myocytes adherent to a basement membrane were significantly lower than attached control myocytes (1.2 +/- 0.2% versus 4.3 +/- 0.3%, and 15 +/- 2 versus 37 +/- 5% resting cell length/sec, respectively; p less than 0.05). Similarly, in the unattached state, the extent and velocity of shortening of SVT myocytes were reduced by over 50% from control values. Contractile properties of attached and unattached cardiocytes were also examined in the presence of 2-8 mM extracellular Ca2+. For both attached and unattached SVT myocytes, responsiveness to increases in extracellular Ca2+ were significantly blunted from control values. Ultrastructural examination of SVT myocytes revealed that the percent volume of myofibrils within isolated myocytes was reduced from control values (46 +/- 7% versus 65 +/- 2%, p less than 0.05). In summary, SVT Cardiomyopathy is probably due to a primary defect in isolated myocyte contractile performance. The reduced contractile function of SVT cardiomyopathic myocytes was associated with abnormalities in cytoarchitecture and Ca2+ responsiveness.

Maully J Shah - One of the best experts on this subject based on the ideXlab platform.

  • a clinical risk score to improve the diagnosis of Tachycardia Induced Cardiomyopathy in childhood
    American Journal of Cardiology, 2016
    Co-Authors: Jeremy P Moore, Maully J Shah, Erin L Albers, Jack C Salerno, Elizabeth A Stephenson, Shuo Wang, Andreas Pflaumer, Richard J Czosek, Jason M Garnreiter, Kathryn K Collins

    Tachycardia-Induced Cardiomyopathy (TIC) is a treatable cause of heart failure in children, but there is little information as to which clinical variables best discriminate TIC from other forms of Cardiomyopathy. TIC cases with dilated Cardiomyopathy (DC) from 16 participating centers were identified and compared with controls with other forms of DC. Presenting clinical, echocardiographic, and electrocardiographic characteristics were collected. Heart rate (HR) percentile was defined as HR/median HR for age, and PR index as the PR/RR interval. P-wave morphology (PWM) was defined as possible sinus or nonsinus based on a predefined algorithm. Eighty TIC cases and 135 controls were identified. Cases demonstrated lower LV end-diastolic diameter and LV end-systolic diameter than DC controls (4.3 vs 6.5, p 130%, PR index >30%, and nonsinus PWM was associated with a sensitivity of 100% and specificity of 87% for the diagnosis of TIC. Model training and validation area under the curves were similar at 0.97 and 0.94, respectively. In conclusion, pediatric TIC may be accurately discriminated from other forms of DC using simple electrocardiographic parameters. This may allow for rapid diagnosis and early treatment of this condition.

  • predictors of myocardial recovery in pediatric Tachycardia Induced Cardiomyopathy
    Heart Rhythm, 2014
    Co-Authors: Jeremy P Moore, Maully J Shah, Payal A Patel, Kevin M Shannon, Erin L Albers, Jack C Salerno, Maya A Stein, Elizabeth A Stephenson, Shaun Mohan, Hiroko Asakai

    Background Tachycardia-Induced Cardiomyopathy (TIC) carries significant risk of morbidity and mortality, although full recovery is possible. Little is known about the myocardial recovery pattern. Objective The purpose of this study was to determine the time course and predictors of myocardial recovery in pediatric TIC. Methods An international multicenter study of pediatric TIC was conducted. Children ≤18 years with incessant tachyarrhythmia, cardiac dysfunction (left ventricular ejection fraction [LVEF] Results Eighty-one children from 17 centers met inclusion criteria: median age 4.0 years (range 0.0–17.5 years) and baseline LVEF 28% (interquartile range 19–39). The most common arrhythmias were ectopic atrial Tachycardia (59%), permanent junctional reciprocating Tachycardia (23%), and ventricular Tachycardia (7%). Thirteen required extracorporeal membrane oxygenation (n = 11) or ventricular assist device (n = 2) support. Median time to recovery was 51 days for LVEF and 71 days for LVEDD. Two (4%) underwent heart transplantation, and 1 died (1%). Multivariate predictors of LV systolic functional recovery were age (hazard ratio [HR] 0.61, P = .040), standardized Tachycardia rate (HR 1.16, P = .015), mechanical circulatory support (HR 2.61, P = .044), and LVEF (HR 1.33 per 10% increase, p=0.005). For normalization of LV size, only baseline LVEDD (HR 0.86, P = .008) was predictive. Conclusion Pediatric TIC resolves in a predictable fashion. Factors associated with faster recovery include younger age, higher presenting heart rate, use of mechanical circulatory support, and higher LVEF, whereas only smaller baseline LV size predicts reverse remodeling. This knowledge may be useful for clinical evaluation and follow-up of affected children.

  • combined inhibition of na and ca2 channels a novel paradigm for the treatment of incessant ventricular arrhythmias in andersen tawil syndrome
    Heart Rhythm, 2014
    Co-Authors: Christopher M Janson, Steven Poelzing, Maully J Shah

    Introduction Andersen-Tawil syndrome type 1 (ATS1), also referred to as long QT syndrome type 7, is a disorder of ventricular repolarization caused by mutations in the KCNJ2 gene. The cardiac phenotype is characterized by bidirectional ventricular Tachycardia (VT), polymorphic VT, and multifocal premature ventricular contractions, with or without corrected QT prolongation. In addition, patients manifest facial dysmorphisms and periodic skeletal muscle paralysis. Treatment of ventricular arrhythmia in ATS1 can be difficult, and patients with a high burden of ventricular ectopy can develop Tachycardia-Induced Cardiomyopathy. In this case report, we describe a novel approach to the treatment of refractory ventricular arrhythmia in an adolescent patient with ATS1.

Motonobu Hayano - One of the best experts on this subject based on the ideXlab platform.

  • a case of Tachycardia Induced Cardiomyopathy due to chronic ectopic atrial Tachycardia
    Clinical Cardiology, 1993
    Co-Authors: Motonobu Hayano, M Tomomro D Kawasaki, M Yoshiki D Egucm, M Shinsuke D Tsuji, M Takasw D Tokushima, M Tohru D Ogata, M Swnji D Eguchi, Moronari Matsunaga, M Kazuyo D Matsunaga

    Only a few reports exist that chronic supraventricular Tachycardia causes ventricular dilation and poor left ventricular contraction—so-called “Tachycardia-Induced Cardiomyopathy.”1-4 Clinical and electrophysiologic features of chronic supraventricular Tachycardia including chronic persistent ectopic atrial Tachycardia (EAT)5-7 in adults have also been described by a few investigators.5-9 We report a rare case of long follow-up of chronic EAT-Induced severe Cardiomyopathy and mitral regurgitation that was well controlled after medical treatment.

Mark D Carlson - One of the best experts on this subject based on the ideXlab platform.

D Mario M D Gonzalez - One of the best experts on this subject based on the ideXlab platform.

  • flecainide suppresses bidirectional ventricular Tachycardia and reverses Tachycardia Induced Cardiomyopathy in andersen tawil syndrome
    Journal of Cardiovascular Electrophysiology, 2007
    Co-Authors: A Oscar M D Pellizzon, Martin Tristanifirouzi, M Luis D Kalaizich, J Louis M D Ptacek, D Mario M D Gonzalez

    Bidirectional ventricular Tachycardia (BVT), although a rare arrhythmia in the general population, is frequently observed in patients with Andersen-Tawil syndrome and long QT interval. However, the pharmacologic treatment of this arrhythmia remains unknown. In the present study, we documented the favorable antiarrhythmic action of flecainide in a young woman with sustained BVT and Andersen-Tawil syndrome. She presented with incessant BVT that could only be terminated with flecainide. During sinus rhythm, a prolonged QT interval was observed. Genetic studies revealed a mutation in the K(+) channel gene KCNJ2. Over a 4-year follow-up period, recurrence of her arrhythmia occurred twice. The first episode was due to noncompliance and resolved with resumption of flecainide therapy. The second recurrence was associated with a Tachycardia-Induced Cardiomyopathy and resolved when the dose of flecainide was increased from 200 to 300 mg daily. This report suggests that flecainide can be effective in controlling BVT associated with Andersen-Tawil syndrome and indicates that the left ventricular dysfunction is secondary to the arrhythmia and not due to an associated phenotypic manifestation of the disorder.