RESUMEN

OBJECTIVE: To test the hypothesis that myocardial stunning is due to myofibrillar oedema. METHODS: Experiments were performed in anaesthetised closed-chest pigs. In 15 pigs (group 1), myocardial stunning was produced by repetitive ischaemia and reperfusion; 5 pigs each were studied at 2 hours, 2 days, and 5 days later. Circumferential left ventricular (LV) mid-wall myocardial strain (E(cc)) was estimated in vivo using tagged magnetic resonance imaging. Myocardial water content (MWC) was measured post mortem, from which interfilament lattice distance (d) was calculated. In 6 pigs (group 2), myocardial dysfunction was produced by intracoronary administration of a mast cell degranulator. Animals were euthanised immediately upon induction of regional LV dysfunction to avoid development of inflammation. In 4 pigs (group 3), transmission electron microscopy (EM) was performed to quantify d in stunned versus normal myocardium. RESULTS: In group 1 pigs, MWC was raised in the stunned compared with normal myocardium (p<0.02) and decreased over time. An inverse relation was found between E(cc) and MWC in the stunned myocardium (r = -0.81) and between E(cc) and d (r = -0.90). A similar relation was noted between wall thickening and increase in MWC in group 2 (r = -0.84) pigs. In group 3 pigs, d on EM was significantly lower (40 (3) nmol/l) in normal myocardium than in stunned myocardium (46.4 (4) nmol/l), p<0.001. CONCLUSIONS: Ischaemia-reperfusion results in myocardial oedema, with consequent myocyte swelling and myofibrillar oedema. The latter leads to an increase in d, causing myosin heads to either fail to latch, or to latch improperly, onto the actin filament with poor force generation, leading to myocardial dysfunction. As the myocardial oedema abates, myocyte function improves.

Asunto(s)

RESUMEN

OBJECTIVE: To determine whether, when the vasomotor capacity of the coronary arterioles is exhausted at rest, myocardial blood volume decreases in order to maintain a normal capillary hydrostatic pressure, even at the expense of myocardial oxygen delivery. METHODS: 18 dogs were studied. In group 1 (n = 9), coronary driving pressure (CDP) was reduced by 10-80 mm Hg below normal by a stenosis; in group 2 (n = 9), it was increased 20-80 mm Hg above baseline by increasing aortic pressure with phenylephrine. Myocardial contrast echocardiography (MCE) was undertaken to measure the myocardial blood volume fraction and myocardial blood flow (MBF). RESULTS: In group 1 dogs, as CDP was reduced, both coronary blood flow (CBF) and MBF decreased. Myocardial blood volume fraction also decreased and myocardial vascular resistance increased, while coronary sinus PO2 decreased. In group 2 dogs, as CDP was increased, epicardial CBF increased but MBF remained unchanged because of a decrease in myocardial blood volume fraction. Myocardial vascular resistance decreased, however, implying the presence of coronary arteriovenous shunting, which was supported by a progressive increase in the coronary sinus PO2. CONCLUSIONS: When arteriolar tone is exhausted so that CBF becomes dependent on CDP, myocardial blood volume decreases in order to maintain a constant capillary hydrostatic pressure, which takes precedence over myocardial oxygen delivery. These novel findings implicate capillaries in the regulation of CBF beyond the autoregulatory range.

Asunto(s)

RESUMEN

BACKGROUND: We hypothesized that by detecting regions with adequate collateral-derived myocardial blood flow (MBF) within the risk area (RA), we could predict ultimate infarct size (IS) at the time of coronary occlusion. METHODS AND RESULTS: Group 1 dogs (n=15) underwent coronary occlusion without reperfusion, whereas group 2 dogs (n=6) underwent both occlusion and reperfusion. RA was measured with aortic root injections of microbubbles. Myocardial contrast echocardiography (MCE) was performed with high mechanical index intermittent harmonic imaging at pulsing intervals (PIs) of <1 to 30 cardiac cycles during an intravenous infusion of microbubbles (Sonozoid). MBF was measured with radiolabeled microspheres, and postmortem tissue staining was used to determine IS. Perfusion defect size (PDS) on MCE varied with the PI and was largest at a PI of 2.6+/-0.4 seconds, where it correlated well with RA (r=0.82). PDS was smallest at a PI of >/=10.6+/-1.5 seconds, where it correlated closely with IS (r>/=0.92). Areas that underwent necrosis could be identified early after coronary occlusion as having the lowest microvascular flow velocity (beta) and MCE-derived MBF (Axbeta). The results were similar with or without reperfusion. Because of variability in collateral-derived MBF, there was no correlation between RA and ultimate IS (P=0.37). The extent of regional dysfunction also correlated poorly with IS (r=0.31). CONCLUSIONS: MCE can be used immediately after coronary occlusion to define ultimate IS by measuring the magnitude and spatial extent of collateral-derived residual MBF within the RA. Thus, it could help individualize risk and management in acute myocardial infarction.

Asunto(s)

Asunto(s)