Table 1.
Parameter | Baseline | Ischemia | Anisotropic |
---|---|---|---|
EDP (mmHg) | 11.3±4.3 | 17.3±6.1† | 15.9±7.5 |
EDV* (ml) | 78.2±15.5 | 89.0±18.0† | 82.2±16.2‡ |
ESP (mmHg) | 96.1±14.8 | 94.7±14.3 | 92.2±9.7 |
ESV* (ml) | 62.7±13.5 | 75.0±17.7† | 66.85±15.4‡ |
SV (ml) | 15.5±3.8 | 14.0±3.9 | 15.4±3.5 |
HR (bpm) | 108±10 | 109±15 | 111±15 |
CO (L/min) | 1.69±0.51 | 1.54±0.54 | 1.70±0.44 |
max dP/dt (mmHg/s) | 1227±337 | 1220±431 | 1342±249 |
Hemodynamic data from 10 dogs that showed a shift in cardiac output curve 45 minutes after coronary ligation. Dogs were pretreated with propranolol and atropine to prevent reflex changes in heart rate and intrinsic myocardial contractility; by design, end-systolic pressure (ESP), heart rate (HR), and maximum dP/dt did not vary significantly during the experiment. During Ischemia, animals compensated for reduced systolic function via the Frank-Starling mechanism, increasing end-diastolic pressure (EDP) and volume (EDV) to maintain stroke volume (SV) and cardiac output (CO) despite increased end-systolic volume (ESV). Anisotropic surgical reinforcement significantly reduced EDV and ESV.
Midwall volumes include cavity volume and approximately half the LV wall volume.
P<0.001 vs. baseline;
P<0.001 vs. ischemia.