Metabolic changes and myocardial injury during cardioplegia: a pilot study.

BACKGROUND: The timing, nature, and severity of both increased cardiac troponin I (cTn-I) levels and myocardial injury during ischemic arrest with cardioplegia are unknown. To define them more accurately, we studied myocardial metabolic activity and the release of markers of myocardial cell injury into the coronary sinus before, during, and after cardioplegia. METHODS: We simultaneously measured creatine kinase, creatine kinase-MB, cTn-I, lactate, phosphate, and blood gases in coronary sinus and systemic arterial blood from 12 patients before cardiopulmonary bypass, after removal of the aortic cross-clamp, and after discontinuation of cardiopulmonary bypass. We also measured coronary sinus flow and transmyocardial fluxes of all analytes and calculated myocardial oxygen consumption, myocardial carbon dioxide production, and myocardial energy expenditure. RESULTS: Myocardial lactate release increased 10-fold after removal of the aortic cross-clamp (p = 0.012) and was accompanied by a surge in myocardial phosphate uptake (p = 0.056). These events were associated with only partial cardioplegia-induced suppression of myocardial oxygen consumption (p = 0.0047), myocardial carbon dioxide production (p = 0.0022), and myocardial energy expenditure (p = 0.0029). Simultaneously, coronary sinus cTn-I levels increased from a mean of 0.76 to 2.43 ng/mL after removal of the aortic cross-clamp, and 2.51 ng/mL after cardiopulmonary bypass (p = 0.014), leading to an increase in arterial cTn-I concentration from 0.18 to 0.98 and 3.01 ng/mL (p = 0.0002). Thus, cTn-I release across the myocardium was absent at baseline, became detectable (p = 0.012) after removal of the aortic cross-clamp, and correlated with cross-clamp and pump times. Similar changes occurred with creatine kinase-MB. CONCLUSIONS: Metabolic myocardial stress occurs during ischemic arrest with cardioplegia and is associated with inadequate suppression of metabolism and with a surge in cTn-I and creatine kinase-MB release, which is maximal after removal of the aortic cross-clamp. These changes are likely to represent structural myocardial cell injury.

Myocardial cell injury in septic shock.

OBJECTIVE: To determine the presence of otherwise undetected myocardial cell injury in patients with septic shock using daily measurements of cardiac troponin I (cTN I). DESIGN: Prospective observational study. SETTING: Intensive care unit of a tertiary institution. PATIENTS: Fifteen consecutive patients with septic shock and six mechanically ventilated patients without septic shock. INTERVENTIONS: Daily collection of blood for the measurement of cTN I serum levels. Regular biochemical and hemodynamic assessment. Illness severity assessment and collection of demographic data. MEASUREMENTS AND MAIN RESULTS: Fifteen patients were studied for a median period of 3 days (range, 1 to 9 days). Serum cTN I concentrations were elevated to values otherwise considered diagnostic of acute myocardial infarction in 12 patients and were significantly higher than in critically ill controls (p = .01). All three patients who died in the intensive care unit and all four patients who did not survive beyond 28 days had elevated levels of cTN I. Survivors tended to lower levels of cTN I while in septic shock than nonsurvivors, and all three patients without increased cTN I survived. There was a significant positive correlation between vasoactive drug requirements and cTN I level (p = .04) and a significant negative correlation between cTN I concentration and left ventricular stroke work index (p = .01). CONCLUSION: Myocardial cell injury appears to be common in patients with septic shock and correlates with cardiac dysfunction.