Progressive loss of myocardial contractile function despite unimpaired coronary blood flow after cardiac surgery.

OBJECTIVE

Mild to moderate transient contractile dysfunction is frequently observed after cardiac surgery on cardiopulmonary bypass (CPB) but may also lead to low-cardiac-output (LCO) failure especially in patients with unstable angina, and is often referred to represent myocardial stunning. Whether time course of contractile dysfunction after cardiac surgery is similar to that of myocardial stunning was investigated in pigs.

METHODS

After baseline measurements of systemic hemodynamics (micromanometry), myocardial contractile function (sonomicrometry), cardiac output and coronary flow (ultrasonic probe), CPB was instituted. Control animals (n = 7) were weaned after 3 h from CPB. In LCO animals (n = 8), global ischemia was induced for 10 min by aortic crossclamping, followed by 1 h of cardioplegic cardiac arrest. After declamping and reperfusion, CPB was terminated after a total of 3 h. Measurements were repeated at 15 min, 4 h and 8 h after CPB. Systemic TNFalpha-plasma concentrations were measured (ELISA) and left ventricular biopsies were analyzed with respect to myocardial TNFalpha (immunohistochemistry) and irreversible cellular damage (light/electron microscopy).

RESULTS

Contractile function decreased in LCO (75 +/- 12%) and control (83 +/-17%) at 15 min compared to baseline (p < 0.05). Thereafter, contractile function remained unchanged in control, but progressively decreased in LCO (52 +/- 12% at 4 h; 36 +/- 5% at 8 h; p < 0.05). Coronary flow remained unchanged in both groups. Cardiac output progressively decreased to 2.8 +/- 0.9 l/min at 8 h in the LCO group compared to baseline (5.9 +/- 1.1 l/min, p < 0.05) and control (5.7 +/- 1.4 l/min, p < 0.05). There was no evidence for myocardial infarction. TNFalpha-plasma concentrations and myocardial TNFalpha-staining were increased at 8 h after CPB in the LCO group compared to baseline and control (p < 0.05).

CONCLUSIONS

The progressive pattern of myocardial dysfunction apart from ongoing ischemia after cardiac surgery suggested underlying mechanisms at least partially different from those of myocardial stunning.