ABSTRACT
OBJECTIVES: This study delineates between infarcts varying in transmurality by using endocardial electrophysiologic information obtained during catheter-based mapping. BACKGROUND: The degree of infarct transmurality extent has previously been linked to patient prognosis and may have significant impact on therapeutic strategies. Catheter-based endocardial mapping may accurately delineate between infarcts differing in the transmural extent of necrotic tissue. METHODS: Electromechanical mapping was performed in 13 dogs four weeks after left anterior descending coronary artery ligation, enabling three-dimensional reconstruction of the left ventricular chamber. A concomitant reduction in bipolar electrogram amplitude (BEA) and local shortening indicated the infarcted region. In addition, impedance, unipolar electrogram amplitude (UEA) and slew rate (SR) were quantified. Subsequently, the hearts were excised, stained with 2,3,5-triphenyltetrazolium chloride and sliced transversely. The mean transmurality of the necrotic tissue in each slice was determined, and infarcts were divided into <30%, 31% to 60% and 61% to 100% transmurality subtypes to be correlated with the corresponding electrical data. RESULTS: From the three-dimensional reconstructions, a total of 263 endocardial points were entered for correlation with the degree of transmurality (4.6 +/- 2.4 points from each section). All four indices delineated infarcted tissue. However, BEA (1.9 +/- 0.7 mV, 1.4 +/- 0.7 mV, 0.8 +/- 0.4 mV in the three groups respectively, p < 0.05 between each group) proved superior to SR, which could not differentiate between the second (31% to 60%) and third (61% to 100%) transmurality subgroups, and to UEA and impedance, which could not differentiate between the first (<30%) and second transmurality subgroups. CONCLUSIONS: The degree of infarct transmurality extent can be derived from the electrical properties of the endocardium obtained via detailed catheter-based mapping in this animal model.
Subject(s)
Cardiac Catheterization/methods , Electric Impedance , Electromagnetic Phenomena/methods , Electrophysiologic Techniques, Cardiac/methods , Fluoroscopy/methods , Myocardial Infarction/diagnosis , Radiography, Interventional/methods , Signal Processing, Computer-Assisted , Animals , Cardiac Catheterization/instrumentation , Disease Models, Animal , Dogs , Electromagnetic Phenomena/instrumentation , Electrophysiologic Techniques, Cardiac/instrumentation , Fluoroscopy/instrumentation , Myocardial Infarction/classification , Predictive Value of Tests , Radiography, Interventional/instrumentationABSTRACT
Allopurinol, a potent inhibitor of xanthine oxidase, is known to effectively protect the heart against damage in patients undergoing cardiac bypass surgery. There is still an ambiguity concerning the presence of xanthine oxidase in the human heart. Thus, the mechanism underlying the protective effect of allopurinol is unclear. Transition metal ions, such as iron and copper, can participate in single-electron reactions and mediate the formation of oxygen-derived free radicals. In this study the interaction between allopurinol and Cu(II) was investigated. Spectrophotometric investigation shows that allopurinol (0-0.8 mM) form a 1:1 complex with Cu(II) ions (0-0.8 mM) with a specific absorbance peak at 364 nm. Also, the rate constant (k) for the copper-catalyzed aerobic oxidation of ascorbate was markedly decreased in the presence of allopurinol (from 0.068 min-1 to 0.014 min-1). Allopurinol substantially reduced the copper-mediated and ascorbate-driven DNA breakage. Spectrophotometric measurements did not indicate a specific interaction between iron ions and allopurinol. It is suggested that the beneficial effects of allopurinol during reperfusion of the heart could stem from its chelation of copper, yielding a complex with low redox activity.
Subject(s)
Allopurinol/therapeutic use , Chelation Therapy , Copper , Coronary Artery Bypass/adverse effects , Myocardial Reperfusion Injury/prevention & control , Ascorbic Acid/metabolism , Humans , Iron , Iron Chelating Agents/therapeutic use , Oxidation-ReductionABSTRACT
The effectiveness of the University of Wisconsin solution on extended myocardial preservation was examined in this study using phosphorus 31-nuclear magnetic resonance spectroscopy. Isolated perfused rat hearts were arrested and stored in four preservation solutions: group 1, modified Krebs-Henseleit solution; group 2, modified St. Thomas' Hospital solution; group 3, oxygenated modified St. Thomas' Hospital solution containing 11 mmol/L glucose; and group 4, University of Wisconsin solution. The changes in myocardial high energy phosphate profiles and the intracellular pH values were measured during 12 hours of cold (4 degrees C) global ischemia and 90 minutes of normothermic reperfusion. Following ischemia, the hearts were assessed for hemodynamic recovery and myocardial water content. During ischemia, adenosine triphosphate depletion was observed in all groups; however, after 5 hours of ischemia, the adenosine triphosphate levels were significantly higher in group 3 compared with the other groups (adenosine triphosphate levels at 6 hours in mumol/gm dry weight: group 3, 7.6; group 4, 3.2; group 2, < 1; p < 0.025). The tissue water content at the end of ischemia was lower with the University of Wisconsin solution compared with the modified St. Thomas' Hospital solution or the oxygenated modified St. Thomas' Hospital solution (in ml/gm dry weight: group 4, 3.0; group 2, 4.4; group 3, 3.9; p < 0.05). The adenosine triphosphate repletion during reperfusion was greater with the University of Wisconsin solution compared with the modified St. Thomas' Hospital solution or the oxygenated modified St. Thomas' Hospital solution (12 mumol/gm dry weight in group 4; 8.1 in group 2; 9.0 in group 3; p < 0.05). Similar findings were obtained for the recovery of left ventricular pressure (in percent of preischemic control: group 4, 70%; group 2, 42%; group 3, 52%; p < 0.01) and coronary flow (group 4, 61%; group 2, 49%; group 3, 49%; p < 0.05). These data suggest that preservation with the University of Wisconsin solution affords improved hemodynamic recovery, enhanced adenosine triphosphate repletion, and reduced tissue edema upon reperfusion; however, oxygenated St. Thomas' Hospital solution with glucose is associated with the preservation of higher myocardial adenosine triphosphate levels during prolonged cold global ischemia. In conclusion, these data indicate that the University of Wisconsin solution might improve graft tolerance of ischemia in clinical heart transplantation.
Subject(s)
Cardioplegic Solutions/pharmacology , Heart/drug effects , Organ Preservation Solutions , Organ Preservation/methods , Solutions/pharmacology , Adenosine , Adenosine Triphosphate/analysis , Allopurinol , Animals , Bicarbonates/pharmacology , Body Water , Calcium Chloride/pharmacology , Glutathione , Heart/physiology , Hemodynamics/drug effects , Hydrogen-Ion Concentration , Insulin , Magnesium/pharmacology , Magnetic Resonance Spectroscopy , Male , Myocardial Ischemia/etiology , Myocardial Ischemia/physiopathology , Myocardium/chemistry , Phosphocreatine/analysis , Phosphorus , Potassium Chloride/pharmacology , Raffinose , Rats , Rats, Sprague-Dawley , Sodium Chloride/pharmacology , Treatment OutcomeABSTRACT
Branched chain amino acids (BCAA) have been found to have a protective effect on the ischemic myocardium. Isolated rat hearts were perfused with phosphate-free Krebs-Henseleit (KH) solution with or without BCAA. A Latex balloon-tipped catheter was inserted into the left ventricle to measure intracavitary pressures. Hearts were subjected to 18 minutes of 'no flow' global ischemia and then reperfused for 30 mins at 37 degrees C. Metabolism of high energy phosphates during ischemia and recovery was studied by P-31 NMR. Intracellular pH was calculated from the chemical shift of Pi. Pressure recovery was better with KH + BCAA (89 +/- 16%) than with KH (41 +/- 26%) (P = 0.0001); dP/dt recovery was also improved with BCAA (84 +/- 19% vs 27 +/- 27% for KH) (P = 0.0003). After 18 mins of ischemia, ATP levels in the BCAA group were higher than in the KH perfused hearts (33 +/- 20 vs 17 +/- 10% of pre-ischemic value) (P = 0.02). No significant difference was found in the intracellular pH at the end of the ischemic period. Following reperfusion the recovery of pH was better in the BCAA group (7.09 +/- 0.06 vs 7.04 +/- 0.06) (P = 0.03). These results show that BCAA protect the heart from myocardial ischemic injury, decrease depletion of ATP during ischemia, and enhance post-ischemic hemodynamic function.
Subject(s)
Amino Acids, Branched-Chain/pharmacology , Coronary Circulation , Heart/drug effects , Adenosine Triphosphate/metabolism , Animals , Blood Pressure , Heart/physiology , Heart Rate , Hydrogen-Ion Concentration , In Vitro Techniques , Magnetic Resonance Spectroscopy/methods , Male , Perfusion , Phosphocreatine/metabolism , Phosphorus , Rats , Rats, Inbred StrainsABSTRACT
Open heart surgery is associated with postoperative sternal pain, which is exacerbated by cough, deep breathing and movement, thus limiting the physical activity of the patient. Transcutaneous electrical nerve stimulation (TENS) was administered to 40 patients suffering from persistent chest pain immediately following open heart surgery, and to ten other patients complaining of pain between three and eight weeks after operation. The efficacy of TENS was assessed by the subjective recordings, analgesic drug requirement, capability to carry out deep inspirations with an "Incentive Deep Breathing Exerciser" apparatus, and repeated chest X-ray examinations. We conclude that TENS is a useful method of pain control and should be used more frequently in patients after open heart surgery, especially in the older patient and in patients with chronic lung disease.