Mary Lee Myers

Biventricular Function in the Adult Respiratory Distress Syndrome: Hemodynamic and Radionuclide Assessment, with Special Emphasis on Right Ventricular Function

We examined biventricular function in patients with the adult respiratory distress syndrome (ARDS) by a combmation of invasively determined pressures and flows and concomitant radionuclide angiography. Right (RVEF) and left (LVEF) ventricular ejection fractions were measured; right and left ventricular end-diastolic (EDVI) and end-systolic (ESVI) volume indices were calculated from the respective ejection fraction and measured ther. modilution stroke volume. With an increase in the outflow pressure load on the right ventricle,measured as the mean pulmonary artery pressure (PAP), the RVEF fell (Y66.25-l.O1X; r2.42; p <.001) and both the RVEDVI (y13.39+3.66X; r�.33; p <.001)and RVESVI (Y = 23.9 + 3.57X; r’ .41; p <.001) increased. Progressive Acute microvascular lung injury, a complication of

Pleuropulmonary morbidity: Internal thoracic artery versus saphenous vein

Although use of the internal thoracic artery (ITA) for coronary artery bypass grafting results in superior graft patency and improved patient survival, our initial clinical observations suggested an increased incidence of pleuropulmonary morbidity with its use. One hundred consecutive patients with left ITA grafts were studied prospectively and compared with a consecutive retrospective group of 100 patients undergoing coronary artery bypass grafting with saphenous vein grafts only. Preoperative, postoperative day (POD) 2, POD 6, and postoperative week 8 chest roentgenograms were analyzed for atelectasis and effusion. Postoperative left lower lobe atelectasis was common in both groups on both POD 2 (saphenous vein, 43%, versus ITA, 53%; not significant) and POD 6 (saphenous vein, 40%, versus ITA, 41%; not significant). There was a significantly higher incidence of pleural effusion on POD 6 in the ITA group (84% versus 47%; p less than 0.05) but most of these were small. There was more chest tube drainage (1,413 versus 1,028 mL; p less than 0.01) and a greater need for secondary thoracostomy or thoracentesis (4% versus 0%) in the ITA group. The left pleural space was opened in 67 of the 100 ITA patients but pleurotomy did not appear to influence postoperative morbidity. We conclude that use of the internal thoracic artery for coronary artery bypass grafting results in a small but significant increase in pleuropulmonary morbidity.

Sodium-hydrogen exchange inhibitors improve postischaemic recovery of function in the perfused rabbit heart

OBJECTIVE The aim was to examine the effects of the Na+/H+ exchange inhibitors amiloride and methylisobutyl amiloride (MIA) in buffer perfused rabbit hearts subjected to one hour of normothermic ischaemia (37 degrees C) followed by reperfusion. METHODS Experiments were carried out in five groups of Langendorff perfused rabbit hearts: (1) control, (2) amiloride, and (3) MIA (agents in both the preischaemic and reperfusion perfusate), (4) amiloride-R and (5) MIA-R (agents added at reperfusion only). Functional evaluation included serial measurement of resting tension, force, rates of ventricular force development and relaxation, and coronary perfusion pressure. Samples of coronary effluent were obtained for creatine kinase assay and hearts were freeze clamped for metabolite assays. RESULTS Reperfusion resulted in a marked increase in resting tension in group (1) which was statistically significant compared to groups (2) and (3). Groups (2) and (3) also showed significantly improved recovery of ventricular force, rate of force development, and rate of ventricular relaxation. Addition of either agent only during reperfusion failed to produce a significant beneficial effect. There were no significant differences among the groups with respect to postreperfusion creatine kinase release or end reperfusion metabolite levels. CONCLUSION This study shows for the first time that both of the Na+/H+ exchange inhibitors amiloride and MIA produce improved recovery of ventricular function in rabbit hearts subjected to ischaemia and reperfusion, although the beneficial effect was not obtained with drug administration at the time of reperfusion only.

Activated neutrophils impair rabbit heart recovery after hypothermic global ischemia

Cardiopulmonary bypass is known to cause neutrophil activation, and activated neutrophils appear to be of importance in myocardial reperfusion injury. This study examined the effect of a preischemic infusion of activated neutrophils on the recovery of myocardial function after 40 minutes of hypothermic global ischemia. Studies were carried out in three groups of Langendorff-perfused rabbit hearts: control, control (unactivated) neutrophil infusion, and phorbol myristate acetate-activated neutrophil infusion. The activated neutrophil group showed significant deterioration in function during the activated neutrophil infusion. All three groups demonstrated significant depression of function initially after reperfusion, but the two control groups subsequently recovered to baseline levels. The activated neutrophil group, however, showed a persistent significant depression in ventricular force, rate of ventricular tension development, and rate of ventricular relaxation as well as a significant increase in coronary vascular resistance. It is concluded that activated neutrophils depress myocardial function and contribute to impaired recovery of function after global hypothermic ischemia.

Endotoxin induces a dose-dependent myocardial cross-tolerance to ischemia-reperfusion injury.

Objective: To test whether or not endotoxin induces a dose‐dependent reduction of myocardial contractile dysfunction after a standardized period of myocardial ischemia and reperfusion and whether nitric oxide is involved in this form of myocardial protection. Design: Prospective, randomized, controlled animal study. Setting: University research laboratory. Subjects: Twenty‐five male Sprague‐Dawley rats. Interventions: After anesthesia, the left carotid artery was cannulated under sterile conditions and animals were allowed to recover from surgery for 12 hrs. Sterile saline or increasing doses (2.5, 5, or 10 mg/kg body weight) of endotoxin (Escherichia coli 026:B6; Sigma, Mississauga, Ontario, Canada) were given intravenously (1 mL over 5 mins). In some rats, diaspirin‐crosslinked hemoglobin (200 mg/kg) was infused 6 hrs and 60 min before endotoxin infusion (10 mg/kg). Hearts were rapidly excised for retrograde perfusion through the ascending aorta (Langendorff apparatus) 6 hrs later. After baseline data collection, hearts were subjected to global ischemia (30 mins, 37°C [98.6°F]), followed by 30 mins of reperfusion. Measurements and Main Results: Physiologic variables were recorded 6 hrs after saline and endotoxin infusion. Baseline myocardial systolic contractility and diastolic compliance were assessed, respectively, by left ventricular developed pressure (LVDP) and left ventricular (LV) volume‐preload relationships. After 30 min of reperfusion, LVDP recovery and left ventricular end‐diastolic pressure were measured. Endotoxin induced LV systolic contractile depression, irrespective of the dose of endotoxin administered. LV diastolic dysfunction varied between different doses of endotoxin administered. On reperfusion, endotoxin produced a dose‐dependent improvement of postischemic LVDP recovery: 30 ± 6% in sham, 78 ± 9% in 2.5 mg/kg, 93 ± 8% in 5 mg/kg, and 107 ± 10% in 10 mg/kg endotoxin heart. In rats treated with 10 mg/kg endotoxin, diaspirin‐crosslinked hemoglobin pretreatment abrogated endotoxin‐induced postischemic LVDP recovery improvement (105 ± 10% vs. 43 ± 7%, p = .01). Conclusion: Sublethal doses of endotoxin induce in a dose‐dependent manner a delayed form of myocardial protection against ischemia. Although free‐cell hemoglobin solution abrogates this endotoxin‐induced cross‐tolerance, we propose that possible mechanisms involved in this form of myocardial protection include nitric oxide pathway activation.

Blunt cardiac trauma: Survival after bichamber rupture

Rupture of cardiac chambers after nonpenetrating blunt thoracic trauma is being recognized with increasing frequency. Despite a high mortality rate, survival after repair of a single-chamber rupture is widely reported. Bichamber cardiac rupture is less frequent, and we report a patient who survived this injury.

Coronary Artery Spasm: A Rare But Important Cause of Postoperative Myocardial Infarction

Myocardial infarction that is attributed to native coronary artery spasm in the early postoperative phase has rarely been documented. We report three cases of postoperative myocardial infarction secondary to angiographically demonstrated coronary spasm. Native coronary artery spasm is a rare, but important cause of postoperative ischemia and infarction. Suspicious electrocardiographic changes warrant consideration of transesophageal echocardiography to detect unexpected wall motion abnormalities. Established treatments include intravenous or intracoronary infusion of nitroglycerin and calcium channel antagonists, although several new therapeutic agents may also be beneficial. Prompt coronary angiography is the only definitive modality for early diagnosis and targeted treatment.