Cellular versus myocardial basis for the contractile dysfunction of hypertrophied myocardium.
Population
Isolated cardiac muscle cells from 7 cats with right ventricular pressure-overload hypertrophy and 7…
Comparison
Right ventricular pressure-overload hypertrophy… vs Sham operation
Design
Preclinical
Authors
Discussion
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Implication
Intrinsic myocyte defect may drive RV hypertrophy dysfunction; leaves open human translation and therapeutic relevance.
Key Points
- To investigate whether contractile dysfunction in hypertrophied myocardium is intrinsic to cardiac muscle cells or influenced by the interstitial environment.
- Cardiac muscle cells isolated from seven right ventricles of pressure-overloaded cats
- Contractile function assessed via laser diffraction under graded viscous loads
- Comparison made with cardiocytes from seven sham-operated cats
- Hypertrophied cardiocytes showed a peak velocity of sarcomere shortening of 2.1 microns/sec (p<0.001) compared to 3.6 microns/sec in controls.
- Maximum sarcomere shortening was 0.14 microns for hypertrophied cells versus 0.21 microns for controls (p<0.001).
- Time to peak shortening was significantly longer in hypertrophied cardiocytes (160.4 msec) compared to controls (150.1 msec, p<0.04).
Structured PICO
P
Population
Isolated cardiac muscle cells (cardiocytes) from 7 cats with right ventricular pressure-overload hypertrophy (via pulmonary artery banding) and 7 sham-operated control cats (total n=14 cats).
I
Intervention
Right ventricular pressure-overload hypertrophy induced by banding the pulmonary artery
C
Comparator
Sham operation
O
Outcome
Contractile function of cardiocytes in response to graded viscous external loads defined by laser diffraction (including peak velocity of sarcomere shortening, maximum extent of sarcomere shortening, time to peak shortening, and relengthening properties)surrogate
This study demonstrates that the contractile dysfunction observed in right ventricular pressure-overload hypertrophy is an intrinsic defect of the cardiac muscle cell itself, rather than solely due to the abnormal interstitial environment.
Cite This Study
Mann et al. (1991) studied this question.