Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0022116 (ischemia)
 91,303 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The authors present the clinical history of a 66 year old woman with a previous anterior myocardial infarction and periinfarct ischemia as well as ischemia in another area not related to the scar (in the posterolateral region of the left ventricle) in whom they successfully performed percutaneous coronary angioplasty of the anterior descending and circumflex arteries since the patient was not a candidate for surgical revascularization because of her clinical condition.
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PMID:[Complex and multiple vessel angioplasty]. 866 23

To investigate the role of left ventricular (LV) diastolic function in the maintenance of exercise capacity in patients with systolic dysfunction, symptom-limited cardiopulmonary exercise testing combined with radionuclide ventriculography was performed in 24 patients with an LV ejection fraction < 35% after anterior myocardial infarction. The ratio of pulmonary artery wedge pressure (PAWP) to LV end-diastolic volume (EDV), an index of global diastolic function, correlated significantly with peak oxygen consumption at peak exercise (r = -0.55; p = 0.006), whereas ejection fraction at peak exercise did not. The change in PAWP/EDV ratio from rest to peak exercise was related to the increases in stroke volume (r = -0.54; p = 0.006) and cardiac output (r = -0.51; p = 0.01) during exercise, but the change in ejection fraction was not. Resting hemodynamics did not differ between patients with preserved exercise capacity (group 1, n = 8) and those with exercise impairment (group 2, n = 16). At peak exercise, stroke volume, cardiac output, and EDV were significantly higher, and PAWP and PAWP/EDV ratio were significantly lower in group 1 than in group 2, but ejection fraction and end-systolic volume were similar in both groups. Although the incidences of hypertension, LV hypertrophy, and infarct-related coronary artery lesions did not differ between the two groups, group 2 had a significantly higher incidence of non-infarct-related coronary artery lesions than group 1 (p < 0.05). Thus in patients with LV systolic dysfunction after anterior myocardial infarction, the major cause of exercise impairment and failure to increase LV performance during exercise was diastolic dysfunction associated with the presence of non-infarct-related coronary artery lesions with the potential for exercise-induced ischemia of the noninfarcted areas.
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PMID:Importance of left ventricular diastolic function on maintenance of exercise capacity in patients with systolic dysfunction after anterior myocardial infarction. 900 95

The present study evaluates the activity of the Na/H antiport during cold ischemia and aims to determine its influence on cellular sodium. pH and volumes. Cellular parameters; volumes, sodium, pH and high energy phosphates, were measured by multinuclear NMR spectroscopy in rat hearts during 12 h of storage at 4 degrees C and reperfusion, along with functional parameters. Cell volumes were measured by 1H and 59Co NMR using the extracellular marker cobalticyanide, pH and energetics by 31P NMR and sodium compartmental distribution by 23Na NMR spectroscopy using the shift reagent Dy(TTHA)-3. Three storage solutions were applied: Krebs-Henseleit (containing 144 mM sodium, KH), a solution supplemented with 0.20 mM amiloride (KH-ami) and a solution containing 23 mM sodium and 242 mM mannitol (KH-man). Inhibition of the Na/H antiport with amiloride reduced the cellular sodium accumulation by 56%. The end-ischemic concentrations were 45 mM (KH-ami) and 77 mM (KH). Amiloride also reduced the extent of cell swelling by 53% from an end-ischemic volume of 3.56 ml/gdw (KH) to 2.97 ml/gdw (KH-ami), however cell swelling persisted in both groups at reperfusion (33% increase in cell water). The molar ratio of sodium and water cellular accumulation was constant: Na/H2O approximately 3.7 x 10(-3) throughout the whole storage period. Inhibition of the antiport was protective for the high energy phosphates during ischemia and reperfusion. In KH-ami the pH acidified after 6 h of storage to an end-ischemic value of 6.35 (pH = 6.50 in KH): this difference persisted after 60 min of reperfusion, pH = 6.98 in KH-ami and pH = 7.1 in KH. Storage in the low-sodium solution was disadvantageous for the high energy phosphates during ischemia and reperfusion with a recovery of pH to 6.92 when reperfused with KH. Hearts stored with amiloride or mannitol solution failed to resume contraction at reperfusion. It is concluded: (a) the antiport is active at 4 degrees C; (b) during ischemia it mediates sodium influx and contributes to cell swelling with minor effects on the cytosolic pH; (c) at reperfusion the antiport is active it participates in the extrusion of excess protons, but has a minor impact on sodium and water homeostasis; (d) inhibition of the antiport does not protect the cardiac muscle at low temperatures.
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PMID:The relation between cellular sodium, pH and volumes and the activity of Na/H antiport during hypothermic ischemia: multinuclear NMR studies of rat hearts. 901 42

A 54-year-old man with a left ventricular free wall rupture following acute anterior myocardial infarction underwent a repair surgery with percutaneous cardiopulmonary support (PCPS). During surgery and postoperatively, PCPS provided sufficient support flow. The patient was successfully weaned from PCPS on the 15th postoperative day and discharged subsequently. In the management of cardiac rupture patients, PCPS has the merit of preventing rupture progression and the advantage of recovery of pulmonary function. However, there are several problems to solve. The support effectiveness and recovery of the patient's heart should be carefully evaluated. Effective left heart decompression also needs to be established. Heparin-coated circuits still need proper anticoagulation treatment to prevent thrombus formation especially while support flow is low. A circuit construction that allows easier maintenance and safer exchange of oxygenators and pump heads is suggested. Ischemia of the cannulated leg should be prevented by femoral artery perfusion.
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PMID:Various problems during long-term percutaneous cardiopulmonary support. 921 55

The electrophysiologic and antifibrillatory properties of tedisamil (KC-8857) were studied in vivo in a conscious canine model of sudden cardiac death. Male mongrel dogs were anesthetized, and surgical anterior myocardial infarction was induced by a 2-h occlusion, with reperfusion of the left anterior descending coronary artery. Three to five days after infarction, dogs were subjected to programmed electrical stimulation (PES) to identify those at risk for ischemia-induced ventricular fibrillation. Previous studies documented that dogs with a significant anterior-wall infarction develop ventricular tachycardia in response to PES and are at an increased risk for sudden cardiac death on imposition of a transient ischemic event in a region remote from the infarct-related artery. PES-inducible animals were randomized to either oral placebo or oral tedisamil treatment (3 mg/kg, b.i.d for 4 days, Group 1, n = 8). Control animals received empty gelatin capsules (Group 2, n = 8). The effective refractory period and QTc interval were unchanged after 3 days of oral placebo or tedisamil dosing. Arrhythmic activity after drug administration was not observed in dogs treated with tedisamil. PES induction of ventricular tachycardia was reduced significantly in the tedisamil-treated group (100% inducible before drug vs. 9% inducible after drug; p < 0.05). In the sudden-cardiac-death protocol, tedisamil reduced the incidence of lethal ischemic arrhythmias developing in response to acute posterolateral myocardial ischemia. Tedisamil-treated animals exhibited a 100% compared with a 25% survival rate in the control group (p < 0.05). Anterior-wall infarct size, expressed as a percentage of the left ventricle, did not differ between groups: Group 1 = 20 +/- 1%; Group 2 = 22 +/- 1%. Our findings suggest that tedisamil might be useful in the prevention of malignant ventricular arrhythmias in myocardial ischemic injury.
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PMID:Antifibrillatory efficacy of long-term tedisamil administration in a postinfarcted canine model of ischemic ventricular fibrillation. 945 78

QT dispersion has been recognized as an undesirable marker because of its association with arrhythmogenicity in patients with myocardial infarction, but the relation between QT interval dispersion and wall motion abnormalities has not been clarified. After the introduction of reperfusion therapy, it was recognized that T waves were inverted twice in the course of myocardial infarction. An investigation was made of the clinical significance of QT dispersion in relation to the presence of inverted T waves and left ventricular wall motion abnormalities in 34 patients (mean age, 59 years) with acute anterior myocardial infarction who underwent successful reperfusion therapy. The amplitude of the deepest inverted T waves occurring within the first 3 days (T1) and after 3 days (T2) of myocardial infarction were measured in electrocardiographic (ECG) lead V3. On the ECGs on which T1 and T2 were recorded, QT dispersion was calculated (QTd1, QTd2), and T1 and T2 were correlated with QTd1 (r = .65) and QTd2 (r = .47), respectively. The difference between the extent of asynergy in the acute phase and the chronic phase, which was evaluated by the centerline method, was correlated with T1 (r = .63) and QTd1 (r = .67). Patients with a QTd1 of 0.1 second or longer showed a greater change in the extent of asynergy (23.4 +/- 13.1% vs 4.9 +/- 9.8%, P < .01) and less asynergy in the chronic phase (19.9 +/- 15.6% vs 46.5 +/- 14.0%, P < .01) than patients with a QTd1 of less than 0.1 second. Thus, QT dispersion in the acute phase of anterior myocardial infarction indicates recovery of left ventricular wall motion. Prolongation of the local action potential duration of the myocardium that recovers from severe ischemia may be a contributor to the increased QT dispersion that results in inversion of T waves in the acute phase of myocardial infarction.
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PMID:Does increased QT dispersion in the acute phase of anterior myocardial infarction predict recovery of left ventricular wall motion? 953 72

Six cases in our institution of various presentations of left anterior descending (LAD) myocardial bridging were found on coronary angiography. Generally a benign condition, this finding can result in ischemia or infarction as seen in some of our cases. We found one case in which the bridge resulted in an anterior myocardial infarction in an elderly patient, one case with fixed stenoses at the entry and exit point of the bridge causing ischemia, another with vasospasm within the bridged segment, one case in which the patient was referred for intervention of a fixed stenosis which after intracoronary nitroglycerin (NTG) was found to be an LAD bridge, another case in which the thallium myocardial perfusion scan revealed a reversible anterior defect, and finally one case with anginal chest pain despite a normal coronary flow reserve proximal and distal to the bridged segment. Our treatments varied from stenting in three patients to medical therapy in the remaining patients. We concluded that a thorough evaluation in this population should include functional testing for ischemia, intravascular ultrasound to assess wall thickness, and coronary flow reserve measurements in order to determine the significance of the these bridges. Stenting may have a role in select patients. However, additional studies are needed.
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PMID:Systolic compression of the left anterior descending coronary artery: a case series, review of the literature, and therapeutic options including stenting. 1197 36

The aims of this study were to compare exercise-induced ST-segment elevation with and without ischemia and to examine the relation between exercise-induced ST-segment elevation and the location of myocardial ischemia. Seventy-nine patients with first anterior myocardial infarction underwent thallium-201 exercise myocardial scintigraphy test one month after myocardial infarction. There were 37 patients showing no reversible defect (non ischemia group), 33 with reversible defect in the territory of the left descending coronary artery (homozonal ischemia group) and 9 with a reversible defect in the territory of the left circumflex or right coronary artery (remote ischemia group). There were no significant differences among the three groups with respect to infarct size, presence of dyskinesis and exercise endurance time. Patients with homozonal ischemia had the highest degree of ST-segment elevation (0.22 +/- 0.09 mV) followed by patients without ischemia (0.13 +/- 0.07 mV) and those with remote ischemia (0.09 +/- 0.08 mV, P <.01). In conclusion, Myocardial ischemia adjacent to infarction amplifies exercise-induced ST-segment elevation.
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PMID:Myocardial ischemia adjacent to infarction enhances the magnitude of exercise-induced ST-segment elevation one month after myocardial infarction. 1212 9

Spontaneous coronary artery dissection is a rare cause of ischemic heart disease, often related with a poor prognosis. We report the case of a 38-year-old woman without cardiovascular risk factors, admitted to our coronary care unit for unstable angina with ECG findings of inferior ischemia. The day after, an acute anterior myocardial infarction occurred and was treated with intravenous thrombolysis. Again, there were ECG signs of transient inferior ischemia. Coronary angiography showed widespread spontaneous coronary dissection involving the terminal left main stem, both the left anterior descending and circumflex artery, and the right coronary artery even peripherally, rendering any type of revascularization procedure inappropriate. The patient was placed on beta-blockers, acetylsalicylic acid and nitrates and her symptoms resolved; the 17-month angiographic follow-up showed almost complete healing of spontaneous coronary artery dissection. The peculiarities of the case are discussed and a review of the literature is provided.
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PMID:Spontaneous coronary dissection of all three coronary arteries: a case description with medium-term angiographic follow-up. 1261 Nov 28

Experimental and clinical evidence documents the beneficial effects of blocking sympathetic activity and modulating heart rate to reduce risk for lethal events in ischemic heart disease. Beside beta-adrenergic receptor blockade, vagal activation is a meaningful approach but not yet easily attainable. Promising results were shown with low-dose atropine and scopolamine, but no follow-up was done because of significant adverse side effects. Pirenzepine is an atropine analogue approved to treat peptic ulcer disease in Europe that is devoid of central actions, which are mostly responsible for anti-muscarinic agents side effects. The vagomimetic action of IV low-dose pirenzepine was studied at rest under control conditions, at rest during acute coronary artery occlusion, and during exercise in conscious dogs with a healed anterior myocardial infarction (MI). The effects of pirenzepine were then compared, by internal control analysis, with those of atenolol (1 mg/kg). Increasing doses of pirenzepine (from 0.01 to 1 mg/kg) were tested in 11 dogs at rest by measuring time and frequency domain heart rate variability (HRV). The most effective dose (0.1 mg/kg) was used in the study. At the most effective dose, pirenzepine increased all measures of time domain HRV by 40-50%. However, the vagomimetic action of pirenzepine was lost during exercise and brief ischemia and no anti-arrhythmic action was observed. Conversely, pirenzepine effectively modulated the heart rate increase during acute ischemia at rest with an effect comparable to that of atenolol. The vagomimetic action of pirenzepine in the acutely ischemic heart supports the possibility that this intervention may be helpful for chronic autonomic modulation in post-MI patients.
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PMID:Autonomic modulation during acute myocardial ischemia by low-dose pirenzepine in conscious dogs with a healed myocardial infarction: a comparison with beta-adrenergic blockade. 1271 96


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