Correlation of Myocyte Lengthening to Chamber Dilation in the Spontaneously Hypertensive Heart Failure (SHHF) Rat

• Published in: Journal of molecular and cellular cardiology Vol. 30; no. 11; pp. 2175 - 2181
• Main Authors: Tamura, Tetsutaro, Onodera, Tatsuyuki, Said, Suleman, Gerdes, A.Martin
• Format: Journal Article
• Language: English
• Published: England Elsevier Ltd 01-11-1998
• Subjects: Animals; Cell Size; Female; Heart failure; Heart Failure - etiology; Heart Failure - pathology; Heart Failure - physiopathology; Hypertension - complications; Myocardial Contraction; Myocardium - pathology; Myocytes; Pathology; Rats; Rats, Mutant Strains; Remodeling; Heart failure; Pathology; Myocytes; Remodeling
• DOI: 10.1006/jmcc.1998.0775
• EISSN: 1095-8584
• ISSN: 0022-2828

Chronic congestive heart failure of various etiologies is characterized by progressive chamber dilation. Although myocyte lengthening is involved, it is not known if this cellular change can account for all of the chamber dilation. The controversy is due largely to technical limitations in collecting data on chamber circumference, myocyte length, and sarcomere length simultaneously. To address this issue, the contributions of myocyte and sarcomere lengthening to progressive chamber dilation in spontaneously hypertensive heart failure (SHHF) rats was examined using a new approach. Female SHHF rats (n=31) were examined at various time points between 2 months of age and the onset of end-stage heart failure (18 months or older). A new method enabled simultaneous collection of data on myocyte length, sarcomere length, and chamber circumference using formalin-fixed tissue. Reliability of cellular measurements was confirmed with an alternate method. LV myocyte length increased linearly between 2 and 24 months of age due to series addition of sarcomeres. Myocyte length increased in direct proportion to chamber circumference during this period (r=0.93,P<0.001). Results suggest that myocyte lengthening alone can account for chamber dilation in the progression to heart failure. Excessive myocyte lengthening is a slow, progressive change that begins long before clinical signs and symptoms of heart failure appear in this model of hypertension and failure. Since myocyte remodeling in hypertensive humans with and without failure is known to resemble that in SHHF rats, these data should provide important insight into chamber dilation and the progression of heart failure in humans.