National surveillance of surgical site infections after coronary artery bypass grafting in Norway: incidence and risk factors.

OBJECTIVE: A mandatory national surveillance system for surgical site infections (SSIs) following certain surgical procedures, including coronary artery bypass grafting (CABG), was introduced in Norway in 2005. The objectives of this study were to measure national baseline incidence rates of SSIs after CABG, describe the characteristics of the patients and procedures, and identify possible risk factors for infection. METHODS: In 2005-2009, all hospitals that performed CABG were invited to assess all patients undergoing CABG surgery in 3-month periods for SSIs. The hospitals evaluated infection status at discharge and 30 days after surgery by sending post-discharge questionnaires to all patients. We calculated incidence proportions and risk ratios for different risk factors. We applied the National Nosocomial Infection Surveillance (NNIS) risk index to the data. RESULTS: In total, 2440 patients were included. Altogether, 124 sternal and 217 harvest site infections were registered, giving incidence proportions of 5.1% and 8.9%, respectively. Over 95% of infections occurred post-discharge from the hospital. No risk factors were identified. Incidence did not significantly increase with higher NNIS risk index; however, 93% of the patients fell into the same risk category. CONCLUSIONS: We have provided a baseline rate for SSIs after CABG procedures in Norway. The results show the importance of post-hospital discharge follow-up. The NNIS risk index did not adequately stratify CABG patients. We recommend that more potential risk variables should be included in the surveillance, such as the European System for Cardiac Operative Risk Evaluation (EuroSCORE), height, weight, and diabetes.

Mechanical restitution curves: a possible load independent assessment of contractile function.

OBJECTIVE: The time constant of mechanical restitution (T((MRC))), proposed to reflect changes in calcium release and uptake, has been shown to increase in left ventricular (LV) failure, and might have a potential as an index of contractile function. However, in vivo studies of the effect on T((MRC)) of changing loading conditions in the normal and failing heart have not been reported. Consequently, in this study, we tested the hypothesis that the increase in T((MRC)) in vivo is independent of preload and afterload. METHODS: Left ventricular pressure-volume loops were assessed at baseline in eight open chest pigs using the combined pressure-volume conductance catheter technique during right atrial pacing at 120b/min. Mechanical restitution curves (MRC) were constructed during four different loading conditions in all eight animals: uninfluenced load, reduced preload (balloon catheter in v. cava inferior), increased afterload (balloon catheter in descending aorta), and increased preload combined with reduced afterload (aortocaval shunting). Acute LV failure was then induced by microembolization through the left main coronary artery, and the experimental protocol was repeated. Contractile response was defined as the maximal first derivative of pressure (dP/dt(max)), and T((MRC)) was calculated using a least square approximation algorithm. RESULTS: Hemodynamic data 30min after microembolization showed decreased mean arterial pressure (98+/-14-67+/-10mmHg, (mean+/-SD) P<0.0001) and dP/dt(max) (1482+/-193-1001+/-125mmHg/s, P=0.001). Stroke volume decreased from 30+/-5 to 20+/-5ml (P<0.0001) compared to baseline, and preload recruitable stroke work decreased from 52+/-7 to 31+/-10mmHg (P=0.002). T((MRC)) increased in all eight animals after induction of LV failure at all loading conditions. There was no difference between the different loading conditions at baseline, nor at LV heart failure, but T((MRC)) increased significantly after the induction of heart failure (ANOVA, two ways). CONCLUSIONS: We have shown that the left ventricular T((MRC)) increases after developed heart failure. The increase in T((MRC)) was independent on loading conditions and thus have a potential for a contractility index.

The pressure-volume loop revisited: Is the search for a cardiac contractility index a futile cycle?

UNLABELLED: Our previous studies indicate that left ventricular end-systolic pressure-volume relations (ESPVRs) or elastance (Ees) are not reduced in studies where expected reductions of contractility should be found (i.e., heart failure, stunning, and endotoxemia). The present study was done to assess whether this phenomenon is due to a particular load sensitivity of elastance, rendering this index inappropriate as a measurement of contractility in pathologic states in vivo. METHODS AND RESULTS: Analysis of previously generated data revealed an increased ESPVR in stunned hearts, in pigs made endotoxemic, and in hearts rapidly paced. After inducing acute heart failure by microembolization, the ESPVR was increased when assessed using linear relations but reduced when assessing ESPVR by a curvilinear algorithm. To further evaluate the effect of different load alterations on ESPVR, this relation was generated by (i) inferior vena caval occlusions (VCOs); (ii) gradually occluding the descending aorta (pressure interventions); and (iii) rapidly infusing blood (120 mL) into the left atrium (volume increments). The load protocol was applied in 5 pigs, before and after the left ventricle was stunned by 11 brief left main coronary artery occlusions/reperfusions (accumulated ischemia 20 min affecting 81% of the left ventricle). Correlation coefficients for left ventricular elastance ranged from 0.93 to 0.99 in all the 3 types of loading interventions. Despite significant reductions in stroke volume, stroke work, and dP/dtmax, VCO-calculated linear and curvilinear Ees increased 90 min after stunning (55% +/- 4% and 94% +/- 6%, respectively). Linear Ees during pressure interventions decreased 36% +/- 1%, whereas curvilinear Ees decreased 33% +/- 3%. During volume infusions, linear Ees decreased 27% +/- 2%. We achieved the same results after blocking the baroreceptor reflexes using hexamethonium. CONCLUSIONS: The Ees is particularly load dependent and will reflect load interventions more than the inotropic state of the cardiac muscle. A VCO-generated Ees increase could be an unmasking of a pronounced preload sensitivity in failing myocardium.

Mechanical restitution curves reflect post-ischemic stunning in pigs.

OBJECTIVES: The time constant of mechanical restitution (T(MRC)), proposed to reflect changes in calcium release and uptake, has been shown to increase in left ventricular (LV) failure. In this study, we tested the hypothesis that T(MRC) also can identify post-ischemic, reversible LV dysfunction (stunning). DESIGN: Stunning was induced by a series of left main coronary artery occlusions in eight anesthetized open chest pigs. Left ventricular pressure-volume relations were assessed using a pressure-volume catheter during right atrial pacing. Mechanical restitution curves (MRCs) were constructed using two different measures of contractile response: maximal first derivative of pressure (CR(dP/dtmax)) and stroke work (CR(SW)). RESULTS: Mean arterial pressure, stroke volume and dP/dtmax were decreased 30 min after stunning. Slopes of end-systolic pressure volume relation and preload recruitable stroke work, however, showed no significant changes after stunning. For MRCs based on CR(dP/dtmax), T(MRC) increased in all eight animals. Using CR(SW), T(MRC) increased in seven out of eight pigs. CONCLUSIONS: Ischemia-reperfusion induce changes in MRCs based on CR(dP/dtmax), and CR(SW). The MRC concept may have potential as a clinical left ventricular performance index.

Pressure-volume-based single-beat estimations cannot predict left ventricular contractility in vivo.

The end-systolic pressure-volume relationship is regarded as a useful index for assessing the contractile state of the heart. However, the need for preload alterations has been a serious limitation to its clinical applications, and there have been numerous attempts to develop a method for calculating contractility based on one single pressure-volume loop. We have evaluated four of these methods. Pressure-volume data were obtained by combined pressure and conductance catheters in 37 pigs. All four methods were applied to 88 steady-state pressure-volume files, including eight files sampled during dopamine infusions. Estimates of single-beat contractility (elastance) were compared with preload-varied multiple-beat elastance [E(es(MB))]. All methods had a low average bias (-0.3 to 0.5 mmHg/ml) but limits of agreement (+/-2 SD) were unacceptably high (+/-2.6 to +/-3.8 mmHg/ml). In the dopamine group, E(es(MB)) showed an increase of 1.7 +/- 0.8 mmHg/ml (mean +/- SD) compared with baseline (P < 0.001). None of the single-beat methods predicted this increase in contractility. It is therefore doubtful whether any of the methods allow for single-beat assessment of contractility.