Hypertrophic Cardiomyopathy. An Electrophysiological Study

Coltart, D J; Meldrum, S. J.

doi:10.1136/bmj.4.5729.217

Cited by 44 publications

(10 citation statements)

References 5 publications

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“…These concentrations are less than onehundredth those reouired in vitro to demonstrate local anaesthetic or cuinidine-like effects on isolated human cardiac muscle fibres (Coltart and Meldrum, 1970). Significant protein binding by plasma would increase this difference.…”

Section: Discussionmentioning

confidence: 78%

Plasma Propranolol Levels Associated with Suppression of Ventricular Ectopic Beats

Coltart¹,

Gibson²,

Shand³

1971

BMJ

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113

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SummaryThe plasma propranolol levels associated with the abolition of chronic, stable ventricular ectopic beats have been studied. Racemic propranolol (DL) suppressed the ectopic foci at plasma levels of 40-85 ng/ml in eight patients, but levels of 70-200 ng/ml were unsuccessful in four patients. Dextro-(D) propranolol levels of 180-310 ng/ml were ineffective in four patients who had previously responded at levels of 60-75 ng/ml of racemic propranolol. The significance of the sympathetic nervous system in the genesis of ectopic beats is discussed. It is concluded that propranolol is clinically effective by virtue of its beta-adrenergic blocking activity.

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Section: Discussionmentioning

confidence: 78%

Plasma Propranolol Levels Associated with Suppression of Ventricular Ectopic Beats

Coltart¹,

Gibson²,

Shand³

1971

BMJ

Self Cite

113

View full text Add to dashboard Cite

show abstract

“…A consistent finding in cardiac hypertrophy is electrical remodelling and, in particular, action potential (AP) prolongation. [1][2][3] Reductions in I to density have been linked to altered AP profiles as well as slowed early repolarization 4 and occur early in cardiac disease, suggesting a possible role for I to changes in hypertrophic process. 5 On a molecular level, cardiac I to is generated by Kv4.2, Kv4.3, and Kv1.4 genes, with their relative contribution varying between species and different regions of the heart.…”

mentioning

confidence: 99%

Prevention of Hypertrophy by Overexpression of Kv4.2 in Cultured Neonatal Cardiomyocytes

et al. 2002

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Background-Prolonged action potentials (APs) and decreased transient outward K ϩ currents (I to ) are consistent findings in hypertrophic myocardium. However, the connection of these changes with cardiac hypertrophy is unknown. The present study investigated the effects of changes in I to and the associated alterations in AP on myocyte hypertrophy induced by phenylephrine. Methods and Results-Chronic incubation of cultured neonatal ventricular rat myocytes (NVRMs) with phenylephrine (PE) reduced I to density and prolonged AP duration, leading to a 2-fold increase in the net Ca 2ϩ influx per beat and a 1.4-fold increase in Ca 2ϩ -transient amplitude. PE treatment of chronically paced (2-Hz) NVRM also induced increases in cell size, protein/DNA ratio, atrial natriuretic factor mRNA expression, as well as ␤/␣ myosin mRNA ratio. These hypertrophic changes were associated with a 2.4-fold increase in activation of nuclear factor of activated T-cells (NFAT), indicating increased activity of the Ca 2ϩ -dependent phosphatase calcineurin. Overexpression of Kv4.2 channels using adenovirus prevented the AP duration prolongation as well as the increases in Ca 2ϩ influx and Ca 2ϩ -transient amplitude induced by PE. Kv4.2 overexpression also prohibited the PE-induced increases in cell size, protein/DNA ratio, atrial natriuretic factor expression, ␤/␣ myosin mRNA ratio, and NFAT activation.Conclusions-Our results demonstrate that PE-mediated hypertrophy in NRVMs seems to require I to reductions and AP prolongation associated with increased Ca 2ϩ influx and Ca 2ϩ transients as well as calcineurin activation. The clinical implications of these studies and the possible involvement of other signaling pathways are discussed. (Circulation.

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“…Although no single ECG pattern is characteristic, abnormal Q waves are one of the most common abnormalities in HCM and can mimic myocardial infarction (5,(12)(13)(14). Despite several electrocardiographic (3,9,11,15), echocardiographic (3,15), electrophysiologic (7,8) and pathologic studies (13,14) the underlying mechanisms of abnormal Q waves in HCM are not yet completely understood. Generally, it has been suggested that Q waves in HCM result from disturbed electrical activation and depolarization of the hypertrophied ventricular septum (5,7,8,13,14).…”

Section: Introductionmentioning

confidence: 98%

“…Patients with hypertrophic cardiomyopathy (HCM) present with various electrocardiographic (ECG) abnormalities, including increased QRS voltage, T wave changes and pathologic Q waves (1)(2)(3)(4)(5)(6)(7)(8)(9)(10)(11). Although no single ECG pattern is characteristic, abnormal Q waves are one of the most common abnormalities in HCM and can mimic myocardial infarction (5,(12)(13)(14).…”

Section: Introductionmentioning

confidence: 99%

“…Despite several electrocardiographic (3,9,11,15), echocardiographic (3,15), electrophysiologic (7,8) and pathologic studies (13,14) the underlying mechanisms of abnormal Q waves in HCM are not yet completely understood. Generally, it has been suggested that Q waves in HCM result from disturbed electrical activation and depolarization of the hypertrophied ventricular septum (5,7,8,13,14). However, no clear correlation between the severity of ventricular hypertrophy and the presence of Q waves could be demonstrated in previous studies (3,15,16).…”

Section: Introductionmentioning

confidence: 99%

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Extent of Myocardial Hyperenhancement on Late Gadolinium-Enhanced Cardiovascular Magnetic Resonance Correlates with Q Waves in Hypertrophic Cardiomyopathy

Papavassiliu¹,

Flüchter²,

Haghi³

et al. 2007

J. of Cardiovascular Magnetic Resonance

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Hypertrophic Cardiomyopathy. An Electrophysiological Study

Cited by 44 publications

References 5 publications

Plasma Propranolol Levels Associated with Suppression of Ventricular Ectopic Beats

Plasma Propranolol Levels Associated with Suppression of Ventricular Ectopic Beats

Prevention of Hypertrophy by Overexpression of Kv4.2 in Cultured Neonatal Cardiomyocytes

Extent of Myocardial Hyperenhancement on Late Gadolinium-Enhanced Cardiovascular Magnetic Resonance Correlates with Q Waves in Hypertrophic Cardiomyopathy

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