Charalampos Pierrakos

Inotropic Agents Improve the Peripheral Microcirculation of Patients With End-Stage Chronic Heart Failure

BACKGROUND Skeletal muscle microcirculation impairment in patients with chronic heart failure (CHF) seems to correlate with disease severity. We evaluated the microcirculation by near-infrared spectroscopy (NIRS) occlusion technique before and after inotropic infusion. METHODS We evaluated 25 patients with stable CHF, 30 patients with end-stage CHF (ESCHF) receiving treatment with intermittent infusion of inotropic agents, and 12 healthy subjects. Thenar muscle tissue oxygen saturation (StO(2)%) was measured noninvasively by NIRS before, during, and after 3-minute occlusion of the brachial artery (occlusion technique) in all subjects and in patients with ESCHF before and after 6 hours of inotropic infusion (dobutamine and/or levosimendan) or placebo (N = 5). RESULTS Patients with ESCHF or CHF presented significantly lower StO(2)% than healthy subjects (74.5% +/- 7%, 78.6% +/- 6%, and 85% +/- 5%, respectively; P = .0001), lower oxygen consumption rate during occlusion (24.6% +/- 8%/min, 28.6% +/- 10%/min, and 38.1% +/- 11.1%/min, respectively; P = .001), and lower reperfusion rate (327% +/- 141%/min, 410% +/- 106%/min, and 480% +/- 133%/min, respectively; P = .002). After 6 hours of inotropic infusion, patients with ESCHF showed significantly increased StO(2)% (74.5% +/- 7% to 82% +/- 9%, P = .001), oxygen consumption rate (24.6% +/- 8%/min to 29.3% +/- 8%/min, P = .009), and reperfusion rate (327% +/- 141%/min to 467% +/- 151%/min, P = .001). No statistical difference was noted in the placebo group. CONCLUSION Peripheral muscle microcirculation as assessed by NIRS is impaired in patients with CHF. This impairment is partially reversed by infusion of inotropic agents in patients with ESCHF.

Comparison of pulsatile with nonpulsatile mechanical support in a porcine model of profound cardiogenic shock.

The aim of this study was to examine whether pulsatility by intraaortic balloon counterpulsation (IABP) is an important adjunct to the treatment of profound cardiogenic shock (CS) with a widely used, nonpulsatile centrifugal pump (CP). In each of 18 anesthetized, open chest pigs, the outflow cannula of the CP was inserted in the aortic arch through the right external carotid artery, and the inflow cannula of the CP was placed in the left atrium. A 40 cc IABP was subsequently placed in the descending aorta through the left external carotid artery. CS was induced by occlusion of coronary arteries and the infusion of propranolol and crystalloid fluid. Mean aortic pressure, pulse pressure, aortic end diastolic pressure, left ventricular end diastolic pressure, right atrial pressure, and heart rate were monitored. Cardiac output and left anterior descending artery flow were measured with a transit time ultrasound flowmeter. During profound CS, life sustaining hemodynamics were maintained only with the support of the assist devices. Hemodynamic support with the CP was associated with a nearly nonpulsatile flow and a pulse pressure of 7 ± 4 mm Hg, which increased to 33 ± 10 mm Hg (p = 0.000) after combining the CP with the IABP. Compared with the hemodynamic support offered by the CP alone, addition of the IABP increased mean aortic pressure from 40 ± 15 to 50 ± 16 mm Hg (p = 0.000), cardiac output from 810 ± 194 to 1,200 ± 234 ml/min (p = 0.003), and left anterior descending artery flow from 26 ± 10 to 39 ± 14 ml/min (p = 0.001). In profound CS, mechanical support provided by a continuous flow CP is enhanced by the added pulsatility of the IABP.

Mechanical Assistance by Intra-Aortic Balloon Pump Counterpulsation During Reperfusion Increases Coronary Blood Flow and Mitigates the No-Reflow Phenomenon: An Experimental Study

The effects of the intra-aortic balloon pump (IABP) counterpulsation on the extent of myocardial infarction (MI), the no-reflow phenomenon (NRP), and coronary blood flow (CBF) during reperfusion in an ischemia-reperfusion experimental model have not been clarified. Eleven pigs underwent occlusion of the mid left anterior descending coronary artery for 1 h, followed by reperfusion for 2 h. CBF, distal to the occlusion site, was measured. In six experiments, IABP support began 10 min before, and continued throughout reperfusion (IABP Group). Five pigs without IABP support served as controls. At the end of each experiment, the myocardial area at risk (MAR) of infarction and the extent of MI and NRP were measured. Hemodynamic measurements at baseline and during coronary occlusion were similar in both groups. During reperfusion, systolic aortic blood pressure was significantly lower in the IABP Group than in controls. In the IABP Group, CBF reached a peak at 5 min of reperfusion, gradually decreased, but remained higher than at baseline, and significantly higher than in controls throughout the 2 h of reperfusion. In controls, CBF increased significantly above baseline immediately after the onset of reperfusion, then returned to baseline within 90 min. The extent of NRP (37 ± 25% vs. 68 ± 17%, P = 0.047) and MI (39 ± 23% vs. 67 ± 13%, P = 0.036), both expressed as percentage of MAR, was significantly less in the IABP group than in controls. After prolonged myocardial ischemia, IABP assistance started just 10 min before and throughout reperfusion increased CBF and limited infarct size and extent of NRP.

Increase in coronary blood flow by intra-aortic balloon counterpulsation in a porcine model of myocardial reperfusion

BACKGROUND Studies of the IABP have reported variable effects on coronary blood flow (CBF). The purpose of the present study was to measure the changes in coronary blood flow induced by intra-aortic balloon pump (IABP) counterpulsation in normal and reperfused porcine myocardium. METHODS A 30-ml IABP was placed in the descending aorta of 6 open-chest pigs. Each pig underwent occlusion of the mid-left anterior descending (LAD) coronary artery for 1 h, followed by reperfusion for 2 h. The effects of IABP support on systolic aortic pressure (SAP) and aortic end-diastolic pressure were recorded. The mean CBF, distal to the LAD occlusion site was measured at baseline and during reperfusion, with and without IABP counterpulsation. RESULTS The IABP decreased SAP and aortic end-diastolic pressure in normal and reperfused myocardium, and maintained a peak aortic diastolic augmentation at the level of SAP. In normal myocardium, the IABP decreased mean CBF by 8.4+/-2.2% (p<0.001). At 2, 15, 30, 60, 90 and 120 min of reperfusion, the IABP increased mean CBF by 11.5+/-6.8%, 8.0+/-7.0%, 11.2+/-6.9%, 12.4+/-12.9%, 23.5+/-9.9% and 8.9+/-6.9%, of the corresponding value without the assistance of the IABP (all p<0.05). CONCLUSIONS In the normal heart, IABP counterpulsation decreased CBF, probably because of a decrease in myocardial oxygen demand from a decreased afterload. During reperfusion the IABP increased CBF, suggesting that it might effectively mitigate the no-reflow phenomenon.

Effects of intra-aortic balloon pump versus centrifugal pump on myocardial energetics and systemic circulation in a porcine model of rapidly worsening acute heart failure

The present experimental study compared the effectiveness of counterpulsation provided by the intra-aortic balloon pump (IABP) versus that of a nonpulsatile, radial-flow centrifugal pump (CFP) in rapidly worsening acute heart failure (HF). Eighteen pigs were included in the study. After the induction of acute moderate HF, circulatory support was randomly provided with either the IABP or CFP. No significant change in cardiac output (CO) and mean aortic pressure (MAP) was observed with either pump. The IABP caused a significantly greater decrease than the CFP in 1) double product (13.138 ± 2.476 mm Hg/min vs. 14.217 ± 2.673 mm Hg/min, p = 0.023), 2) left ventricular systolic pressure (LVSP, 100 ± 8 mm Hg vs. 106 ± 10 mm Hg, p = 0.046), and 3) end-diastolic aortic pressure (EDAP, 70 ± 6 mm Hg vs. 86 ± 6 mm Hg, p = 0.000). The effects of both pumps on total tension time index and LAD flow were similar. After the induction of severe HF, the IABP had its main effects on afterload and decreased LVSP from 88 ± 6 mm Hg to 78 ± 9 mm Hg, (p = 0.008), and EDAP from 57 ± 9 mm Hg to 49 ± 14 mm Hg, (p = 0.044), whereas the CFP exerted its effects mainly on preload, lowering LV end-diastolic pressure from 19 ± 5 mm Hg to 11 ± 4 mm Hg, (p = 0.002). CO and MAP were similarly increased by both assist systems. The IABP (by lowering afterload) and CFP (by lowering preload) both offered significant mechanical support in acute HF. However, afterload reduction offered principally by the IABP seems preferable for the recovery of the acutely failing heart.

Effects of l-NAME on coronary blood flow, infarct size and the extent of the no-reflow phenomenon

BACKGROUND NOS inhibitors are a potential treatment for patients with cardiogenic shock during acute myocardial infarction. Despite hemodynamic efficacy, their effects on the extent of myocardial infarction (MI) and the no-reflow phenomenon (NRP) have not been clarified. METHODS Sixteen pigs underwent occlusion of the mid left anterior descending coronary artery for 1h followed by reperfusion for 2h. Coronary blood flow (CBF), distal to the occlusion site, was measured. In eight experiments, L-NAME (non selective NO synthetase inhibitor) administration began 10 min before the onset of reperfusion and continued for 2h (loading dose 1mg/kg, perfusion rate: 1mg/kg/h) (L-NAME group). Eight pigs received similarly normal saline (controls). At the end of each experiment, the myocardial area at risk (MAR) and extent of MI and NRP were measured. RESULTS Hemodynamics at baseline and during ischemia were similar in both groups. During reperfusion, the mean aortic blood pressure was significantly higher in the l-NAME group. In both groups, CBF reached a peak at 5 min of reperfusion, (no difference between groups). CBF gradually returned to baseline levels within 60 min of reperfusion in both groups. No statistically significant differences in the extent of the NRP (51.8 ± 19.7 vs 60.9 ± 11.4 p=0.35) and MI (77.9 ± 13.9 vs 77.1 ± 8.8 p=0.92), both expressed as a percentage of MAR, were observed between the L-NAME group and the control group. CONCLUSIONS L-NAME administration started immediately before and maintained throughout reperfusion has no effect on NRP and MI size. L-NAME might stabilize patients with post-MI cardiogenic shock without adverse effects on infarct size.