Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0151744 (myocardial ischemia)
 31,282 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Transmyocardial laser revascularization (TMLR), a new technique, provides direct perfusion of ischemic myocardium via laser-created transmural channels. From 1995 to 1996, we treated 7 patients (mean age 60 years, all men) with TMLR. Preperatively, 5 patients were in angina class (C. C. S) 3-4 and 2 patients had unstable angina. To identify the location and extent of their reversible ischemia, the coronary angiogram, 99mSPECT and/or dobutamine echocardiography was performed before operation in 7 patients. Through a left anterior thoractomy in the fifth intehcostal space, heart exposure was gained. With the use of a 700-watt CO2 laser, TMLR was performed on the beating heart. An average of 22 +/- 3 channels were created in 45 minutes with a total operative time of less than 2 and half hours. The in hospital mortality was one of 7 patients. Follow-up ranged from 2 to 12 months (accumulated 48 patient-months). Postoperatively, the relief of angina was noted in 6 patients. Postoperative SPECT and dubatamin-UCG were obtained at 3, 6, and 12 months. (99mTc) SPECT showed a significant improvement of myocardial perfusion in the area of reversible ischemia. Dobutamin-UCG documented an increase in the ventricular wall motion and LVEF in 2 patients as compared with basline. These early results indicate that TMLR may provide angina relief, improve myocardial perfusion and increase cardiac function for patients with ischemic heart disease.
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PMID:[Clinical application of transmyocardial laser revascularization]. 1067 53

Transmyocardial laser revascularization (TMLR) is currently applied to provide clinical benefits in the patients with end-stage coronary artery disease. However, this method is so far indicated only for chronic status of ischemic heart disease. In this study, we have investigated in the canine model whether acute ischemic myocardium could be reperfused by TMLR using CO2 laser. A CO2 laser was used to create transmural myocardial channels. The ischemic areas of 3 cm in diameter were created on the left ventricle with multiple coronary ligations. Laser procedure was carried out 30 minutes after coronary ligation in TMLR group (n = 6), while laser treatment was not performed after coronary ligation in acute myocardial infarction (AMI) group (n = 6). The level of MB isozyme of creatinine kinase (CK-MB) derived from coronary sinus was measured at 0, 3, 6, 12, 18, 24, and 48 hours after coronary ligations, and the pattern of serial CK-MB changing was analyzed. Animals were sacrificed 48 hours after treatment and histologically investigated. The time to peak level of CK-MB in TMLR group appeared significantly earlier (13.0 +/- 2.4 hours) than that in AMI group (22.0 +/- 3.1 hours). The value of CK-MB of 24 hours after ligation in TMLR group (1985 +/- 805 IU/L) was significantly lower than that in AMI group (4759 +/- 778 IU/L). The channels on the gross section after 48 hours of TMLR were patent with some of fibrin network. Red blood cells were scattered in the lumens. It was suggested that acute ischemic myocardium was directly reperfused through the open laser channels from the left ventricular chamber in the canine model.
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PMID:Reperfusion in acute ischemic myocardium by transmyocardial revascularization using CO2 laser. 1075 5

Transmyocardial laser revascularization (TMLR) using a CO2 laser is clinically attempted in end-stage ischemic heart disease that is not treated by conventional bypass grafting or transluminal angioplasty. Besides, clinical trials of TMLR using a Ho:YAG laser have started recently. In this study, we compared the degree of damage to normal myocardium using these 2 types of lasers. Hearts of adult mongrel dogs were exposed under general anesthesia. Dogs were divided into 2 groups; those with channels made in the left ventricle by CO2 laser (CO2 group, n = 5) and those with channels made by Ho:YAG laser (Ho:YAG group, n = 5). The chest was temporarily closed, then serum MB isozyme of creatinine kinase (CK-MB) and troponin T (TnT) were measured sequentially. Twenty-four hours after laser irradiation, hearts were isolated for pathological studies with hematoxylin-eosin and Masson's trichrome stains. The CO2 group produced CK-MB with a peak of 1162.2 +/- 462.2 IU/l and the Ho:YAG group 1804.0 +/- 992.4 IU/l after 12 hours, and there was a significant difference between two groups (p < 0.01). The CO2 group produced TnT with a peak of 1.2 +/- 0.4 ng/ml and the Ho:YAG group 11.6 +/- 4.1 ng/ml after 6 hours, and the peak value in Ho:YAG group was significantly higher than that in the CO2 group (p < 0.001). Thirty channels were confirmed histologically in the CO2 group, and the width of thermal damage layer around the channel lumen was 249 +/- 83 microns. Twenty-seven channels were confirmed histologically in the Ho:YAG group, and the width of thermal damage layer was 760 +/- 288 microns. Thermal damage in the Ho:YAG group was significant greater than that in the CO2 group (p < 0.01). We concluded that TMLR using a CO2 laser is more suitable for end-stage myocardial ischemia than a Ho:YAG laser in terms of myocardial damage.
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PMID:Experimental investigations on relationships between myocardial damage and laser type used in transmyocardial laser revascularization (TMLR). 1075 7

The purpose of this study was to test a new prototype pulsed CO2 laser to be used for transmyocardial laser revascularization (TMR). We wanted to determine whether it can reduce thermal damage and mitigate induced ischemia with improvement in contractile reserve of the heart as evidenced by contrast echocardiography at rest and under dobutamine stress. TMR is an emerging surgical strategy for treatment of myocardial ischemia not amenable to conventional percutaneous or surgical revascularization. Eleven pigs underwent ameroid occluder placement at the origin of the circumflex coronary artery. Six weeks later, occlusion of the circumflex coronary artery was documented. TMR was then carried out on 10 pigs by using a prototype pulsed CO2 laser that delivered 8-12 joules in 1.5 ms with a spot size of 1 mm. Six weeks after TMR, the pigs were restudied. The animals developed significant ischemia after 6 weeks of ameroid occlusion, at rest (p = 0.01) and at peak stress (p = 0.004). Wall motion for the ischemic segments improved significantly 6 weeks after TMR at peak stress (p = 0.02). TMR results in an improvement in wall motion in our model of chronic ischemia and improves wall motion score index more during induced stress than at rest.
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PMID:Effects of transmyocardial laser revascularization by using a prototype pulsed CO2 laser on contractility and perfusion of chronically ischemic myocardium in a porcine model. 1111 Feb 83

Adenosine acts as a cardioprotective agent by producing coronary vasodilation, decreasing heart rate and by antagonizing the cardiostimulatory effect of catecholamines; adenosine also exerts a direct negative inotropic effect. Myocardial ischemia is known to be associated with enhanced levels of adenosine, increased protein kinase C (PKC) activity and prostacyclin (PGI2) release. The present study was conducted to determine if myocardial ischemia alters the cardioprotective effect of adenosine by increasing PKC activity and PGI2 release in the isolated rat heart perfused at 10 ml/min with Krebs-Henseleit buffer (KHB; 95% O2+5% CO2). Adenosine (10 mmol/min) reduced myocardial contractility as indicated by a decrease in contractility (dp/dtmax), heart rate (HR) and coronary perfusion pressure (PP). In hearts subjected to 30 min of ischemia (without perfusion) and then reperfused with KHB, adenosine failed to decrease dp/dtmax, HR or PP. However, during infusion of PKC inhibitor H-7 (1-(5-Isoquinolinesulfonyl)-2-methylpiperazine hydrochloride) (H-7; 6 mmol/min), which commenced 10 min before ischemia and continued throughout reperfusion, adenosine produced a decrease in dp/dtmax, HR and PP, similar to that before ischemia. Infusion of the PKC activator phorbol 12,13-dibutyrate (PDBu; 2 nmol/min) but not an inactive analogue in non-ischemic hearts prevented the adenosine induced decrease in dp/dtmax. During infusion of H-7, PDBu failed to block the direct negative inotropic effect of adenosine in non-ischemic hearts. In addition, pretreatment with H-7 or indomethacin (cyclooxygenase inhibitor) significantly reduced the PGI2 release following ischemia. This data suggest that PKC and PGI2 regulate the direct negative inotropic effect of adenosine, which is abolished during ischemia.
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PMID:Adenosine induced direct negative inotropic effect is abolished during global ischemia: role of protein kinase C and prostacyclin. 1113 71

The short-term benefits of minimal access techniques include less pain, early mobilization, and shorter hospital stay. Nonetheless, significant data have accumulated regarding the complications associated with laparoscopic techniques, including those that are unique to laparoscopic surgery such as bile duct injury and disruption of major blood vessels. Other problems such as myocardial ischemia and respiratory acidosis are associated with the cardiopulmonary effects of pneumoperitoneum and systemic CO2 absorption. These physiologic changes, although tolerated by healthy patients, could have particular adverse consequences for infirm and critically ill patients. It would appear that minimizing IAP during insufflation decreases the risk of potentially marked cardiovascular changes and regional blood flow alterations. In turn, this could arguably decrease the risk of perioperative myocardial events, or organ dysfunction or failure. Laparoscopy in the critically ill patient is questionable because the role is not established. An ICU patient has little to gain from the benefits of early mobilization. Conversely, in the presence of raised ICP or borderline organ function, the physiologic changes associated with pneumoperitoneum and laparoscopy could have profound detrimental effects.
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PMID:Physiologic changes during laparoscopy. 1124 11

Results of transmyocardial laser revascularisation (TMLR) of the myocardium are analyzed. Two types of laser equipment were used domestic laser high-energy CO2 synchronized with patient's ECG, and XeCl laser Max-20. 32 patients underwent TMLR as a single method of surgical correction of the disease, 15 in combination with other methods of myocardium revascularisation. Obtained data testify that TMLR is a highly effective procedure in selective patients with IHD. Results confirm necessity of differential surgical policy for ischemic heart disease that permits to use adequate method of myocardium revascularisation for each patient.
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PMID:[Surgical treatment of ischemic heart disease by transmyocardial laser revascularization]. 1158 25

A moderate reduction in coronary blood flow results in decreased myocardial oxygen consumption, accelerated glycolysis, decreased pyruvate oxidation, and lactate accumulation. To quantitatively understand cardiac metabolism during ischemia, we have developed a mechanistic, mathematical model based on biochemical mass balances and reaction kinetics in cardiac cells. By numerical solution of model equations, computer simulations showed the dynamic responses in glucose, fatty acid, glucose-6-phosphate, glycogen, triglyceride, pyruvate, lactate, acetyl-CoA, and free-CoA as well as CO2, O2, phosphocreatine/creatine, nicotinamide adenine dinucleotide (reduced form)/nicotinamide adenine dinucleotide (oxidized form) (NADH/NAD+), and adenosine diphosphate/adenosine triphosphate (ADP/ATP). When myocardial ischemia was simulated by a 60% reduction in coronary blood flow, the model generated myocardial concentrations, uptakes, and fluxes that were consistent with experimental data from in vivo pig studies. After 60 min of ischemia the concentrations of glycogen, phosphocreatine, and ATP were decreased by 60%, 75%, and 50%, respectively. With the onset of ischemia, myocardial lactate concentration increased and the myocardium switched from net consumer to net producer of lactate. Our model predicted a rapid 13-fold increase in NADH/NAD+, but only a twofold increase in the ratio of acetyl-CoA to free-CoA. These findings are consistent with the concept that pyruvate oxidation is inhibited during ischemia partially by the rise in NADH/NAD+.
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PMID:Mechanistic model of myocardial energy metabolism under normal and ischemic conditions. 1196 72

Although numerous studies have provided evidence that the inflammatory cytokines TNF-alpha and IL-1beta have significant negative inotropic effects, the role of the interleukins in burn-mediated cardiac dysfunction has not been defined. Furthermore, most studies examining the cardiotoxic effects of inflammatory cytokines have ignored the complex inflammatory milieu that occurs in the intact subject with trauma, sepsis, or ischemic heart disease. Therefore, this study examined the time course of IL-1beta and IL-6 secretion by cardiomyocytes after burn trauma, and additional studies examined the effects of these cytokines alone or in combination with TNF-alpha on cardiac contractile performance (Langendorff). Sprague-Dawley rats were given a full thickness burn injury over 40% of the total body surface area; fluid resuscitation was lactated Ringers solution, 4 mL/kg per burn percentage of burn area. Sham burn animals received identical anesthesia and handling, but no burn injury. Rats were sacrificed at several different times postburn, and isolated hearts (n = 4-5 rats/group/time period) were perfused with collagenase-containing buffer to prepare cardiomyocytes or were perfused in vitro to examine cardiac contractile function (n = 5-6 rats/group/time period). Additional naive control rats (n = 10) were included to prepare cardiomyocytes that, in turn, were challenged with different concentrations of either IL-1beta, IL-6, or TNF-alpha alone or in combination for several time periods (CO2 incubator at 37 degrees C for 1-3 h). Finally, inflammatory cytokines alone or in combination were added to the perfusate of hearts isolated from additional control rats (n = 6-7/group) to assess the cardiac contraction and relaxation effects of cytokine challenge. Despite aggressive fluid resuscitation, burn trauma produced a time-related increase in cardiomyocyte secretion of IL-1beta, IL-6, and TNF-alpha. Exposure of naive cardiomyocytes prepared from control rats to each cytokine alone or combined cytokine challenge produced a time-dependent and concentration-dependent decrease in cell viability and an increase in supernatant creatine kinase levels. Either IL-1beta or TNF-alpha produced greater cardiac defects than IL-6 when added separately to Langendorff-perfused hearts; dysfunction was maximal with combined cytokine challenge (IL-1beta plus TNF-alpha plus IL-6). The data confirm that burn trauma upregulates inflammatory cytokine secretion by cardiomyocytes and suggest that these inflammatory cytokines act in concert to produce burn-mediated cardiac contractile dysfunction.
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PMID:IL-1beta and IL-6 act synergistically with TNF-alpha to alter cardiac contractile function after burn trauma. 1239 81

Accumulation of carbon dioxide (CO2) can disturb systemic and cerebral hemodynamics in patients receiving electroconvulsive therapy (ECT). The purpose of this study was to identify the effects of end-tidal CO2 monitoring on hemodynamic changes in patients who received ECT under propofol anesthesia. ECT was prescribed to 40 patients under propofol anesthesia. Ventilation was assisted using a face mask and 100% oxygen, with or without end-tidal CO2 monitoring. Heart rate was significantly increased in patients without end-tidal CO2 monitoring at 1 to 5 minutes after electrical stimulation (p < 0.01). Mean arterial blood pressure and middle cerebral artery blood flow velocity in the group without end-tidal CO2 monitoring were significantly larger than the values in the group with the monitor at 1 to 5 minutes after electrical stimulation. Arterial CO2 tension in the group without end-tidal CO2 monitoring was larger than the value in the group with the monitoring at 1 minute (45+/-5 mm Hg with the monitor and 56+/-8 without the monitor) and 5 minutes (37+/-4 mm Hg with the monitor and 51+/-8 without the monitor) after electrical stimulation (p < 0.01). Application of end-tidal CO2 monitoring is considered beneficial for safe and effective anesthesia management of patients undergoing ECT, especially patients with an intracranial disorder or ischemic heart disease.
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PMID:End-tidal carbon dioxide monitoring stabilized hemodynamic changes during ECT. 1262 Dec 74


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