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

To clarify the optimal management and delineate the characteristics of patients with severe left main disease and cardiogenic shock as a result of an acute anterolateral myocardial infarction (left main shock syndrome), we analyzed the course of 13 such patients from September 1989 to June 1997. Of the 13 patients, 7 (53.8%) were managed with emergency coronary angioplasty (group A), 3 (23.1%) were treated with emergency coronary angioplsty following coronary bypass graft surgery (group B) and 3 (23.1%) underwent emergency coronary bypass graft surgery alone (group C). The interval from the beginning of myocardial ischemia to revascularization was 266 +/- 303 min. The degree of diameter stenosis found in the left main coronary artery was 98.1 +/- 1.8%. Overall in-hospital mortality for the 13 patient with left main shock syndrome was 76.9% (group A: 7/7; group B: 1/3; group C: 2/3, NS) and operative mortality was 61.5% (group A: 6/7; group B: 0/3; group C: 2/3, p = 0.03). When all 13 patients were examined together, the presence of ventricular tachycardia (VT) x ventricular fibrillation (Vf) was found to be the most powerful univariate predictor of operative death (p = 0.03). This is, 7 (87.5%) of the 8 patients with VT x Vf at presentation died within 30 postoperative days, and only 1 (20%) of the 5 patients without VT x Vf died (p = 0.03). Age, percent stenosis of the left main or right coronary arteries, the interval from the beginning of myocardial ischemia to revascularization, intubation, systolic pressure, fractional shortning, pulmonary artery pressure, pulmonary capillary wedge pressure, coronary risk factors, pulmonary edema, mitral regurgitation and percutaneous cardiopulmonary support failed to attain univariate significance at the P = .1 level. The postoperative peak CPK level was 15665 +/- 6710 IU/1 in operative death compared to 4733 +/- 2749 IU/1 in operative survival (p = 0.01). In conclusion, emergency coronary angioplasty following coronary bypass graft surgery for left main shock syndrome has been a very successful therapeutic option. Finally, for the entire group of 13 patients with left main shock syndrome, VT x Vf significantly decreased short-term survival.
 ...
PMID:[Prognosis and management in patients with left main shock syndrome--emergency PTCA following CABG]. 1003 32

We retrospectively analysed the perioperative course of 22 patients who underwent emergency CABG for severe left main trunk lesion. The causes of LMT lesion were spontaneous acute myocardial infarction in 14 patients and failed coronary intervention and coronary angiography in 8 patients. IABP was used preoperatively in all patients and additional coronary perfusion catheter were induced for two patients and PCPS was for one patient. Overall incidence in-hospital operative mortality was 22.7% (5/22), four of them were due to cardiac related causes and one of them was due to acute renal failure. Postoperative level of max CPK enzyme was significantly higher in death cases compared to survivors, 6,330 +/- 3,649 versus 1,299 +/- 1,417 IU/dl. We considered that the most important factors in surgical strategy for acute coronary syndrome with LMT lesion were as follows: improvement of hemodynamics with mechanical cardiac support by IABP or/and PCPS, protection of broad myocardial ischemia using coronary perfusion catheter and urgent surgical revascularization by emergency CABG.
 ...
PMID:[Emergency CABG for patients with LMT lesion treated by mechanical cardiac support]. 1044 50

Cardiac abnormalities in birth asphyxia were first recognised in the 1970s. These include (i) transient tricuspid regurgitation which is the commonest cause of a systolic murmur in a newborn and tends to disappear without any treatment unless it is associated with transient myocardial ischemia or primary pulmonary hypertension of the newborn (ii) transient mitral regurgitation which is much less common and is often a part of transient myocardial ischemia, at times with reduced left ventricular function and, therefore, requires treatment in the form of inotropic and ventilatory support (iii) transient myocardial ischemia (TMI) of the newborn. This should be suspected in any baby with asphyxia, respiratory distress and poor pulses, especially if a murmur is audible. It is of five types (A to E) according to Rowe's classification. Type B is the most severe with respiratory distress, congestive heart failure and shock. Echocardiography helps to rule out critical left ventricular obstructive lesions like hypoplastic left heart syndrome or critical aortic stenosis. ECG is very important for diagnosis of TMI, and may show changes ranging from T wave inversion in one lead to a classical segmental infarction pattern with abnormal q waves. CPK-MB may rise and echocardiogram shows impaired left ventricular function, mitral and/or tricuspid regurgitation, and at times, wall motion abnormalities of left ventricle. Ejection fraction is often depressed and is a useful marker of severity and prognosis. Treatment includes fluid restriction, inotropic support, diuretics and ventilatory resistance if required (v) persistent pulmonary hypertension of the newborn (PPHN). Persistent hypoxia sometimes results in persistence of constricted fetal pulmonary vascular bed causing pulmonary arterial hypertension with consequent right to left shunt across patent ductus arteriosus and foramen ovale. This causes respiratory tension and right ventricular failure with systolic murmur of tricuspid, and at times, mitral regurgitation. Treatment consists of oxygen and general care for mild cases, ventilatory support, ECMO and nitric oxide for severe cases. Cardiac abnormalities in asphyxiated neonates are often underdiagnosed and require a high index of suspicion. ECG and Echo help in early recognition and hence better management of these cases.
 ...
PMID:Cardiac abnormalities in birth asphyxia. 1095 39

Transitory myocardial ischemia (TMI) is seen as a complication of severe asphyxia. Its presentation is variable, ranging from tachypnea to cardiogenic shock, and it is often masked by the predominant disease. The objective of this study was to detect TMI secondary to perinatal asphyxia in a population of asphyxiated newborns (NB) in comparison with asphyxiated NB with no evidence of TMI. From April 1996 to December 1997, 43 asphyxiated (stressed) NB were studied. Three were excluded. Patients were placed into two groups: Group A with TMI (n = 33) and Group B without TMI (n = 7). No significant differences were found in gestational age, birth weight, extrauterine age, Apgar score, or total creatine phosphokinase values between the two groups. Differences were found in CPK-MB levels and in ischemic electrocardiographic changes and blockages, especially for Group A. In this group, only 24 (72.7%) were cardiovascularly symptomatic. We conclude that TMI secondary to perinatal asphyxia is more frequent than has been reported. Thus, it would be useful in all asphyxiated NB to measure CPK-MB isoenzyme activity and patients can then be submitted to an electrocardiogram for detection in order to offer opportune treatment when required.
 ...
PMID:Detection of transitory myocardial ischemia secondary to perinatal asphyxia. 1106 79

Cardiac abnormalities in birth asphyxia were first recognised in 1970s. These include (i) transient tricuspid regurgitation which is the commonest cause of a systolic murmur in a newborn and tends to disappear without any treatment unless it is associated with transient myocardial ischemia or primary pulmonary hypertension of the new born (ii) transient mitral regurgitation which is much less common and is often a part of transient myocardial ischemia, at times with reduced left ventricular function and therefore, requires treatment in the form of inotropic and ventilatory support, (iii) transient myocardial ischemia (TMI) of the newborn. This should be suspected in any baby with asphyxia, respiratory distress and poor pulses especially if a murmur is audible. It is of five types (A to E) according to Rowe's classification. Type B is the most severe with respiratory distress, congestive heart failure and shock. Echocardiography helps to rule out critical left ventricular obstructive lesions like hypoplastic left heart syndrome or critical aortic stenosis. ECG is very important for diagnosis of TMI, and may show changes ranging from T wave inversion in one lead to a classical segmental infarction pattern with abnormal q waves. CPK-MB may rise and echocardiogram shows impaired left ventricular function, mitral and/or tricuspid regurgitation, and at times, wall motion abnormalities of left ventricle. Ejection fraction is often depressed and is a useful marker of severity and prognosis. Treatment includes fluid restriction, inotropic support, diuretics and ventilatory resistance if required, (v) persistent pulmonary hypertension of the new born (PPHN). Persistent hypoxia sometimes results in persistence of constricted fetal pulmonary vascular bed causing pulmonary arterial hypertension with consequent right to left shunt across patent ductus arteriosus and foramen ovale. This causes respiratory distress and cyanosis (sometimes differential). Clinical examination also reveals evidence of pulmonary arterial hypertension and right ventricular failure with systolic murmur of tricuspid and, at times, mitral regurgitation. Treatment consists of oxygen and general care for mild cases, ventilatory support, ECMO and nitric oxide for severe cases. Cardiac abnormalities in asphyxiated neonates are often underdiagnosed and require a high index of suspicion. ECG and Echo help in early recognition and hence better management of these cases.
 ...
PMID:Cardiac abnormalities in birth asphyxia. 1112 17

The changes in systemic circulation during hyperthermic isolated lower limb perfusion with carboplatin and interferon-beta were investigated in 19 patients with malignant melanoma. The cardiac output (CO) increased significantly (p < 0.01) from 3.81 +/- 0.22 L/min before the procedure to 5.30 +/- 0.49 L/min 1 h after hyperthermic perfusion. The double product (mean arterial pressure x heart rate) also increased significantly (p < 0.01) from 5,145 +/- 372 mm Hg/min to 6,760 +/- 486 mm Hg/min. In some patients, it increased to more than twice the control value. These changes were accompanied by an increase in body temperature, presumably caused by the systemic leakage of both warmed blood and interferon-beta. Blood chemistry data demonstrated no significant changes in the liver or renal function. However, the serum CPK level increased markedly on the first postoperative day, and persisted for 1 week, thus suggesting that some muscle damage occurred during the procedure. There was no operative death or severe complications. From these data, we concluded that hyperthermic isolated limb perfusion with interferon-beta is a relatively safe therapeutic method for malignant melanoma of the extremities. However, care should be taken in patients with ischemic heart disease who may suffer a heart attack due to the rapid increase in cardiac work during the procedure.
 ...
PMID:Systemic effects of hyperthermic isolated lower limb perfusion with carboplatin and interferon-beta. 1116 57

Angiotensin II (Ang II) and apoptosis contribute significantly to myocardial ischemia-reperfusion (I-R) injury. Evidence indicates that Ang II may activate apoptosis in myocytes. The present study was undertaken to investigate the effects of angiotensin receptor blockers (ARBs), candesartan, on the apoptosis of cardiac myocytes in rats after I-R. Rats were divided into a control group, a candesartan group I (0.015 mg/kg), and a candesartan group II (0.03 mg/kg). Candesartan was intravenously administered 30 min before ischemia. All rats were subjected to 30 min of coronary occlusion followed by 3 h of reperfusion. The data showed that left ventricular (LV) systolic pressure and LV +dp/dt was decreased after administration of candesartan, but increased after reperfusion in the candesartan group II, compared with those in the candesartan group I and control group. LV -dp/dt was decreased after candesartan administration in candesartan group II. The number of apoptotic cells in the candesartan groups (497+/-204 and 543+/-254, respectively) was higher than that in the control group (287+/-166; p<0.05). There was no significant difference in infarct size among the three groups. However, plasma CPK was lower in the candesartan groups than in the control group. Northern blot analysis showed that p53 mRNA was upregulated in the candesartan groups, in association with increased expression of bax mRNA. Immunohistochemical analysis showed that p53 and bax immunoreactivity were increased in both of the candesartan groups. In conclusion, candesartan increased apoptosis in the rat hearts after acute I-R, and this increase was possibly mediated by upregulation of p53 and bax gene expressions. In addition, candesartan was shown to improve LV function, in association with reduction of CPK release.
 ...
PMID:An angiotensin II type 1 receptor blocker, candesartan, increases myocardial apoptosis in rats with acute ischemia-reperfusion. 1140 58

The diagnosis and clinical significance of blunt cardiac injury remains controversial. Cardiac troponin I is not found in skeletal muscle and has a high sensitivity for myocardial ischemia or injury. We hypothesized that normal troponin levels 4 to 6 hours postinjury would effectively exclude the diagnosis of cardiac contusion. A prospective evaluation of all blunt trauma patients older than 16 and admitted with the possible diagnosis of blunt cardiac injury was undertaken. Patients in whom this diagnosis was considered had an electrocardiogram (EKG) on admission, serum troponin, CPK and isoenzymes 4 to 6 hours postinjury, and admission with overnight telemetry. Other laboratory data and radiographic imaging was obtained as indicated. Seventy-two patients met criteria for entry into the study. Data was incomplete or inaccurately obtained on six patients, and they were excluded. Forty patients had normal troponins and normal EKG's on admission and were discharged the following day without any untoward effect. Sixteen patients were admitted with abnormal EKGs. All of these 16 patients had normal troponins 4 to 6 hours after their injury. They all did well and were discharged the following day. Ten patients had elevated troponins 4 to 6 hours after injury. One died two days later from refractory cardiogenic shock. Another was noted to have severely depressed left ventricular function by echocardiography. The other eight patients sustained no cardiac sequelae and were discharged once recovered from injuries. In the hemodynamically stable patient a normal troponin 4 to 6 hours after injury excludes clinically significant blunt cardiac injury. This holds true whether the admission EKG is normal or not. An elevated troponin does not definitively diagnose a clinically significant contusion. However, these patients should be monitored at least for 24 hours. Patients suspicious for cardiac contusions who have normal troponins and no other serious injuries may be safely discharged to go home from the emergency department.
 ...
PMID:The usefulness of serum troponin levels in evaluating cardiac injury. 1156 57

Recent studies have shown that growth hormone (GH) deficiency may deteriorate post-ischemic myocardial reperfusion damage. Furthermore, GH has been reported to be a promising therapeutic option in the treatment of chronic myocardial dysfunction. However, the exact mechanisms of action of GH on the cardiovascular system, particularly in the acute setting, are still unclear. The aim of our study consisted of monitoring the acute effects of GH infusion on isolated blood-perfused rabbit heart according to dose-response pattern and during ischemic conditions to test its anti-ischemic property. Seven blood-donors perfused isolated hearts were used as experimental model. The mechanical and metabolic data of the isolated organs were continuously monitored. Under aerobic conditions, dose-response curves were initially tested after intracoronary infusion of GH at increasing dosages (1, 2, 3 mg/l). After a stabilization period, the effects of GH infusion (5 mg/kg) administered 30 minutes prior to acute global myocardial ischemia (30 minutes) were also investigated. At the doses tested, GH did not induce any changes either in the developed or in the diastolic pressures of the isolated organ. However, transient reduction of the coronary perfusion pressure was observed at the dosage of 3 mg/l. During the ischemia/reperfusion study, at the dosages used in this study, GH did not modify either the degree of stunning in the early reperfusion or the recovery of the developed pressure at the end of reperfusion. In addition, GH did not prevent either the increase of diastolic pressure during ischemia or the release of lactate and CPK during reperfusion. Tissue content of high-energy phosphates was also not changed by GH infusion. In our experimental model, acute GH infusion did not reduce the ischemic/reperfusion damage of the myocardium. However, GH transiently induced coronary vasodilation without modifying the myocardial contractility. Acute effects of GH appear, therefore, to predominantly relate to vascular dilation suggesting that the effects on myocardial contractility may require long-lasting intake being likely linked to enhancement of specific protein synthesis or gene expression of cardiac myocytes.
 ...
PMID:Preliminary observations on the effects of acute infusion of growth hormone on coronary vasculature and on myocardial function and energetics of an isolated and blood-perfused heart. 1260 25

The hemodynamic effects of high-frequency jet ventilation (HFJV), synchronized with diastole, and intermittent positive-pressure ventilation (IPPV) were studied in 10 dogs with acute right-sided myocardial ischemia and elevated right ventricular pressure. Myocardial ischemia was produced by ligation of the proximal right coronary artery (RCA), then the right ventricular pressure was elevated to facilitate the ischemia by banding the main pulmonary artery. Before and 1, 2, 3, and 5 hr after the RCA ligation, cardiorespiratory variables for each ventilatory mode and creatine phosphokinase MB isoenzyme (CPK-MB) were measured. During HFJV compared with IPPV: there were significant increases in stroke index and left ventricular stroke work index at all ischemic periods, and decreases in peak and mean airway pressures and pulmonary vascular resistance at all ischemic periods, and in the product of systolic right ventricular pressure and heart rate at 2 hr, 3 hr, and 5 hr. The difference in mean airway pressure between IPPV and HFJV correlated significantly with those in cardiac index and stroke index (r = 0.575 and 0.779, respectively). CPK-MB was significantly greater at 3 hr and 5 hr than that before RCA ligation. These findings suggest that HFJV synchronized with diastole offers hemodynamic advantages over IPPV to ischemic right ventricle with constricted pulmonary artery, mainly due to lowering the mean airway pressure.
 ...
PMID:Hemodynamic effects of high-frequency jet ventilation in dogs with acute right coronary arterial ligation and pulmonary arterial banding. 1523 79


<< Previous 1 2 3 4 5 6 Next >>