Cardiac valve surgery and myocardial damage: the role of cardiac troponin I.

AIM: The study investigated the release of cardiac Troponin I (cTnI) levels in heart valve surgery and in coronary artery bypass grafting (CABG). The aims of the research were 1) to evaluate the ability of cTnI to detect the myocardial damage; and 2) to demonstrate possible causative factors of the cTnI release after valve surgery. METHODS: A prospective, single-center study. Ninety consecutive patients were operated on for different types of cardiac surgery; 45 patients underwent cardiac valve surgery - The VALVE group. 45 patients underwent CABG surgery - the CABG group. CTnI levels were measured preoperatively, on the day of operation and the 7 days postoperatively. The diagnosis of damaged myocardium classically performed through the measurement of cTnI, twelve-lead electrocardiograms (ECG) and echocardiographics according to the protocol of the study. RESULTS: Although more elevated cTnI release was noticed in valve group early after operation, no occurrence of cardiac events was found in that group. Statistically significant occurrence of cardiac events was found in CABG group (P=0.015). No relationship was shown between the peak of cTnI and the presence of cardiac events in valve group. A statistically significant correlation was observed between cardiac events and peak cTnI in CABG group (P=0.05). Possible correlations were investigated between the peak of cTnI and perioperative parameters in both two groups. CONCLUSION: The absence of cardiac events and the association of valve surgery with higher early release of cTnI compared to CABG suggest that the type of surgery strongly affects the induction of myocardial damage.

Early mortality and morbidity of bilateral versus single internal thoracic artery revascularization: propensity and risk modeling.

OBJECTIVES: We examined whether bilateral internal thoracic artery (BITA) revascularization is associated with any increased in-hospital mortality and complications compared with single internal thoracic artery (SITA) revascularization. BACKGROUND: Despite proven long-term benefits, BITA revascularization has been slow to be adopted because of fear of increased early morbidity. METHODS: We evaluated 1,697 consecutive patients undergoing BITA (n = 867) or SITA (n = 830) revascularization. We used propensity score analyses and adjusted risk models to address differences between arms. RESULTS: There were 20 (2.3%) deaths in the BITA group versus 26 (3.1%) in the SITA group (odds ratio 0.73, p = 0.30). Propensity analysis identified several parameters that affected the decision to use BITA. Adjusting for propensity score and all potential risk factors, the odds ratio for death with BITA versus SITA was practically 1. Bilateral internal thoracic artery revascularization did not increase the number of in-hospital complications with the possible exception of deep sternal wound infections (11 [1.3%] vs. 3 [0.4%], p = 0.057). In multivariate modeling BITA increased the risk of deep sternal wound infections only in emergent cases and in older patients; the excess risk was negligible among 1,206 patients (71.1% of total) who did not have emergent revascularization and were < or =70 years old (risk difference 0.3%, p = 0.74). There was no difference in length of stay after adjustment for propensity factors (mean 11.3 vs. 11.7 days, p = 0.66). CONCLUSIONS: Bilateral internal thoracic artery revascularization grafting confers no increased risk for early death and does not prolong hospital stay. The small increase in the risk of deep sternal wound infections does not affect the majority of patients.

Impaired platelet aggregation after cardiopulmonary bypass in man: enhancement of collagen-induced aggregation in whole blood and plasma by adrenaline ex vivo.

1. We tested the effect of intravenous adrenaline at 0.55-1.10 nmol min-1 kg-1 (for 3-8 min, at 7-10 min post bypass; n = 7) on both microaggregation in hirudinized whole blood, using platelet counting, and macroaggregation in platelet-rich plasma, using optical aggregometry. Control (n = 12) blood samples were taken before and at 10 and 20 min after bypass. 2. Post-bypass plasma adrenaline levels (nmol/l) increased slightly in controls (1.0 versus 0.7 at 10 min, medians; P = 0.05) and markedly with adrenaline infusion (36 versus 0.5 before infusion, P = 0.02). Microaggregation (percentage decrease in single platelets) in stirred blood, reflecting largely ADP-dependent 'spontaneous' aggregation, was not influenced by adrenaline infusion. In contrast, collagen (0.2 microgram/ml)-induced microaggregation in blood was enhanced by adrenaline (92% versus 41%, P = 0.02), with no change in controls (60% versus 53%, P = 0.61). 3. In controls, collagen (0.6 microgram/ml)-induced macroaggregation in platelet-rich plasma (extent of increase in light transmission, cm) was impaired at 10 min post bypass (5.3 versus 12.1 before bypass, P = 0.01), but was enhanced by adrenaline (7.0 versus 3.6 before infusion, P = 0.02). Platelet counts (x 10(9)/l) were decreased postbypass (155 versus 220, P = 0.02) and were not influenced by adrenaline infusion (167, P = 0.93).(ABSTRACT TRUNCATED AT 250 WORDS)

Macroaggregation of platelets in plasma, as distinct from microaggregation in whole blood (and plasma), as determined using optical aggregometry and platelet counting respectively, is specifically impaired following cardiopulmonary bypass in man.

We determined changes in platelet aggregability following cardiopulmonary bypass, using optical aggregometry to assess macroaggregation in platelet-rich plasma (PRP), and platelet counting to assess microaggregation both in whole blood and PRP. Hirudin was used as the anticoagulant to maintain normocalcaemia. Microaggregation (%, median and interquartile range) in blood stirred with collagen (0.6 micrograms/ml) was only marginally impaired following bypass (91 [88, 93] at 10 min postbypass v 95 (92, 96] prebypass; n = 22), whereas macroaggregation (amplitude of response; cm) in PRP stirred with collagen (1.0 micrograms/ml) was markedly impaired (9.5 [8.0, 10.8], n = 41 v 13.4 [12.7, 14.3], n = 10; p < 0.0001). However, in PRP, despite impairment of macroaggregation (9.1 [8.5, 10.1], n = 12), microaggregation was near-maximal (93 [91, 94]), as in whole blood stirred with collagen. In contrast, in aspirin-treated patients (n = 14), both collagen-induced microaggregation in whole blood (49 [47, 52]) and macroaggregation in PRP (5.1 [3.8, 6.6]) were more markedly impaired, compared with control (both p < 0.001). Similarly, in PRP, macroaggregation with ristocetin (1.5 mg/ml) was also impaired following bypass (9.4 [7.2, 10.7], n = 38 v 12.4 [10.0, 13.4]; p < 0.0002, n = 20), but as found with collagen, despite impairment of macroaggregation (7.2 [3.5, 10.9], n = 12), microaggregation was again near-maximal (96 [93, 97]). The response to ristocetin was more markedly impared after bypass in succinylated gelatin (Gelofusine) treated patients (5.6 [2.8, 8.6], n = 17; p < 0.005 v control), whereas the response to collagen was little different (9.3 v 9.5).(ABSTRACT TRUNCATED AT 250 WORDS)