Key result
Pressure overload elicits concentric hypertrophy to normalize systolic wall stress, whereas volume overload triggers eccentric hypertrophy to reduce diastolic wall stress.
This hindsight article highlights the enduring relevance of the 1975 discovery that pressure and volume overload induce distinct patterns of myocardial hypertrophy driven by different wall stress profiles.
Pressure and volume overload results in concentric and eccentric hypertrophy of cardiac ventricular chambers with, respectively, parallel and series replication of sarcomeres. These divergent patterns of hypertrophy were related 40 years ago to disparate wall stresses in both conditions, with systolic wall stress eliciting parallel replication of sarcomeres and diastolic wall stress, series replication. These observations are relevant to clinical practice, as they relate to the excessive hypertrophy and contractile dysfunction regularly observed in patients with aortic stenosis. Stress-sensing mechanisms in cardiomyocytes and activation of cardiomyocyte death by elevated wall stress continue to intrigue cardiovascular scientists.
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Grossman et al. (2013) conducted an editorial in Left ventricular hypertrophy and aortic stenosis. Pressure overload elicits concentric hypertrophy to normalize systolic wall stress, whereas volume overload triggers eccentric hypertrophy to reduce diastolic wall stress.
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