What question did this study set out to answer?

To identify the ionic mechanisms through which mechanical stretch induces arrhythmias in single ventricular myocytes from normal and hypertrophied hearts.

December 1, 2000Cardiovascular ResearchOpen Access

Stretch-activated currents in ventricular myocytes: amplitude and arrhythmogenic effects increase with hypertrophy

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Population

Ventricular myocytes isolated from human failing hearts, guinea-pig hearts, and rat hearts

Comparison

Local stretch applied between a patch electrode… vs Unstretched state and comparison between…

Design

Preclinical

Authors

AKAndre KamkinPirogov Russian National Research Medical University

Discussion

Member takes

Implication

Greater I(SAC) sensitivity in hypertrophied/failing myocytes may promote arrhythmias; hypothesis-generating for mechanisms but leaves open clinical translation.

Key Points

To identify the ionic mechanisms through which mechanical stretch induces arrhythmias in single ventricular myocytes from normal and hypertrophied hearts.
Isolated single ventricular myocytes from human failing hearts, guinea-pig hearts, and rat hearts (young, old, and old spontaneously hypertensive models).
Applied mechanical stretch using a patch electrode and glass stylus during whole-cell voltage-clamp and current-clamp recordings.
Local mechanical stretch prolonged action potential duration, depolarized resting membrane potential, triggered extra systoles, and activated a gadolinium-sensitive (5 μM Gd3+) non-selective cation current (I(SAC)).
Stretch sensitivity of I(SAC) was 75 pA/μm in young rats (3 months), 143 pA/μm in old rats (15 months), 306 pA/μm in hypertrophied spontaneously hypertensive rats, 262 pA/μm in failing human myocytes, and 143 pA/μm in guinea pigs.

Structured PICO

Population

Ventricular myocytes isolated from human failing hearts, guinea-pig hearts, and rat hearts (young 3-month, old 15-month, and hypertrophied from old 15-month spontaneously hypertensive animals)

Intervention

Local stretch applied between a patch electrode and a glass stylus

Comparator

Unstretched state (relaxation) and comparison between hypertrophied vs. control myocytes

Outcome

Electrophysiological changes including action potential duration, resting membrane potential, extra systoles, and stretch-activated current (I(SAC)) amplitude and sensitivitysurrogate

Local stretch activates arrhythmogenic non-selective cation currents in ventricular myocytes, with heightened sensitivity in hypertrophied and failing hearts, providing a cellular mechanism for stretch-induced arrhythmias.

Cite This Study

Andre Kamkin (2000) studied this question.

synapsesocial.com/papers/6a70127eac440176ef28b844 https://doi.org/10.1016/s0008-6363(00)00208-x

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Implication

Greater I(SAC) sensitivity in hypertrophied/failing myocytes may promote arrhythmias; hypothesis-generating for mechanisms but leaves open clinical translation.

Stretch-activated currents in ventricular myocytes: amplitude and arrhythmogenic effects increase with hypertrophy

Discussion

Member takes

Implication

Key Points

Structured PICO

Cite This Study

Stretch-activated currents in ventricular myocytes: amplitude and arrhythmogenic effects increase with hypertrophy

Discussion

Member takes

Implication

Key Points

Structured PICO

Cite This Study

Also Consider

Also Consider