Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0022116 (ischemia)
 91,303 document(s) hit in 31,850,051 MEDLINE articles (0.01 seconds)

We present clinical and electrophysiological data on 9 patients with paroxysmal reciprocating sinus tachycardia (PRST) of whom only 6 described palpitations. Sinus node disease was present in 5 and cardiac ischemia and/or hypertension in another 3; the remaining case had apparently coincidental Wolff-Parkinson-White (WPW) syndrome. PRST could be initiated in all cases, and terminated in the 4 in whom it was sustained, by suitably timed atrial premature beats over a zone that was dependent on the effective atrial extrastimulus coupling interval (A1-A2) in the high right atrium (HRA). The sequence of atrial depolarization during PRST was similar to that of sinus beats although minor changes in both the P wave and the configuration of the HRA electrogram were observed in half the cases. During paroxysms, cycle length variation and sensitivity to alterations in vagal tone were common. In 6, paroxysms could be initiated by moderately rapid atrial pacing. Repetitive attacks were usually initiated by increases in the sinus rate and not be an antecedent premature atrial extrasystole. Verapamil suppressed sinus node reentry in 5 patients while small doses of atropine favored initiation in 3. PRST was seen in association with AV reentry tachycardias in the patient who had the WPW syndrome.
Eur J Cardiol
PMID:Paroxysmal reciprocating sinus tachycardia. 59 Feb 95

The bioelectrical activity of the heart during repolarization is analysed with Frank leads in a spatial vector model. After physical work most of the test persons showed an amplification of the repolarization vector. It is discussed whether the amplification of the T-vector after physical work should be interpreted as an indication of subendocardial ischemia.
Basic Res Cardiol
PMID:[Vector analysis of the repolarization phase in the exercise-ecg with Frank leads (author's transl)]. 60 29

Sixty-five patients were studied with stress electrocardiography and thallium-20 1 relative myocardial perfusion scintigraphy. Results were correlated with selective coronary angiography. Scintigraphy was more sensitive (85 versus 67 percent), more specific (89 versus 63 percent) and significantly more accurate (87 versus 65 percent) than stress electrocardiography for the diagnosis of significant coronary arterial lesions in patients with isoelectric S-T segments at rest. Stress scintigraphy helped clarify the equivocal stress test due to left bundle branch block, left ventricular hypertrophy, drugs, hyperventilation and other conditions and was more accurate than the stress electrocardiogram (89 versus 53 percent) even in the presence of a depressed S-t segment at rest. Thallium-20 1 scintigraphy is a safe and simple noninvasive method for identifying abnormal myocardial perfusion, stress-induced ischemia and, indirectly, significant coronary arterial lesions.
Am J Cardiol 1978 Jan
PMID:Thallium-20 1 myocardial perfusion scintigraphy for the clinical clarification of normal, abnormal and equivocal electrocardiographic stress tests. 62 4

To determine whether the extensive myocardial injury associated with cardiogenic shock in some patients results from a progressive rather than a discrete massive insult, a study was made of 15 selected patients who had cardiogenic shock within 48 hours of admission, 5 patients with hypovolemic shock without myocardial infarction and 11 patients with myocardial infarction without shock. Peak plasma MB creatine kinase (CK) activity was significantly higher in the seven patients with cardiogenic shock associated with initial infarction (213 international units [IU]/liter) than in patients with shock and previous infarction (98 IU/liter) and in patients with uncomplicated myocardial infarction (125 IU/liter). A prolonged time to peak MB CK activity (averaging 26 hours) and a plateau of elevated MB CK activity were seen in patients with shock associated with initial infarction. Because shock itself did not slow the rate of apparent MB CK disappearance, results obtained suggest that cardiogenic shock associated with initial infarction in selected patients results from progressive myocardial damage underlying continuing release of MB CK into the circulation. The findings are compatible with the concept that, in these patients, cardiogenic shock reflects a vicious cycle of spreading myocardial injury, progressive compromise of cardiac function, exacerbation of ischemia and perpetuation of myocardial damage.
Am J Cardiol 1978 Mar
PMID:Progressive nature of myocardial injury in selected patients with cardiogenic shock. 62 24

Guinea-pig and dog heart mitochondria were isolated in a KEA-medium. Ca2+-transport across mitochondrial membranes was measured continuously with an Aminco Dual-Wavelength-Spectrophotometer and murexide as a Ca2+-sensitive indicator. Ischemia was produced by cardioplegia at 15 degrees C according to Bretschneider. Guinea-pig heart mitochondria as well as mitochondria from dog heart show a spontaneous Ca2+-release without nonphysiological influence. Addition of 3.5 M Na+ can induce a very quick release of Ca2+ taken up by heart mitochondria. This release is different from that occurring spontaneously. Progressive ischemia results in a marked depression of Ca2+-uptake and spontaneous Ca2+-release.
Basic Res Cardiol
PMID:Ca2+-uptake and -release phenomena from cardiac mitochondria under normal and ischemic conditions. 65 15

Insulin was administered to two patients whose diminished myocardial contractility made it difficult to terminate cardiopulmonary bypass. In both instances, bypass was successfully terminated shortly after the insulin injection. These clinical observations led to experiments under the controlled conditions provided by the isolated, working rat heart preparation. The recovery of contractility after 30 minutes of severe ischemia was assessed in all 11 control and 11 insulin-treated hearts. Myocardial performance, as judged by the product of heart rate and peak systolic blood pressure, was significantly greater in the insulin-treated hearts. These clinical observations and experimental findings suggest the need for more extensive study of the potential value of insulin in treating depressed contractility after prolonged myocardial ischemia.
Am J Cardiol 1978 Jun
PMID:Insulin therapy for depressed myocardial contractility after prolonged ischemia. 66 28

The extent to which alterations in the coronary blood flow influence left ventricular (LV) diastolic compliance and wall thickness was studied in isolated, isovolumic (balloon in LV), blood perfused dog hearts. Studies were performed at a ventricular volume which was associated with an LV systolic pressure of 100 mm Hg and changes in LV diastolic pressure (at this constant volume) were taken as changes in LV diastolic complicance. When coronary perfusion pressure was reduced to zero (5 min of global ischemia), LV diastolic wall thickness fell from 9.9 +/- 0.9 mm to 9.2 +/- 0.7 mm (P less than 0.01) and LV diastolic pressure fell only 1.3 mm Hg (from 5.5 +/- 1.0 mm Hg to 4.2 +/- 1.1 mm Hg P less than 0.01). In contrast to these findings in 'near normal' ventricles, global ischemia in severely injured hearts (with unphysiologically high diastolic pressures) resulted in marked reductions in diastolic pressure. Thus, moment to moment changes in coronary blood flow can result in alterations in the diastolic properties of the LV. However, these are extreme interventions, and in the clinical setting, changes in coronary dynamics are unlikely to cause significant changes in LV diastolic pressure.
Eur J Cardiol 1978 Jun
PMID:The influence of acute alterations in coronary blood flow on left ventricular diastolic compliance and wall thickness. 66 59

Ninety-seven patients with a prior transmural myocardial infarction who underwent coronary angiography and treadmill stress testing were studied retrospectively to assess the reliability of the exercise electrocardiogram in detecting additional disease in patients with a prior infarction. In patients with a previous inferior wall infarction, the S-T response to the treadmill stress test had a high degree of sensitivity (87 percent) and specificity (90 percent) in detecting additional significant coronary artery disease. However, in patients with a previous anteroseptal wall infarction, the S-T response had much less sensitivity (52 percent), but the degree of specificity remained high (90 percent). In this group a positive test suggested the presence of ischemia in the lateral or inferoposterior region of the myocardium, or both. A negative S-T response was of little value in distinguishing among groups of patients with single or multiple vessel coronary artery disease. The presence of an anterior ventricular aneurysm is most likely responsible for this low sensitivity rate because it generates an opposing force to the ischemic vector, thereby cancelling the S-T segment changes and producing a false negative treadmill stress test. The resting surface electrocardiogram proved useful in predicting a false negative exercise test. The presence of Q waves in the precordial leads extending to lead V4 or beyond decreased the sensitivity rate of treadmill stress testing to 33 percent.
Am J Cardiol 1978 Jul
PMID:Comparison of S-T segment changes on exercise testing with angiographic findings in patients with prior myocardial infarction. 67 32

The progressive transmural electrographic, biochemical and ultrastructural changes as a function of time after acute coronary occlusion were systematically assessed in eight dogs. Transmural plunge electrodes with poles 1 mm apart were placed in the ischemic and nonischemic zones, and coronary occlusion was maintained for 4 hours. Transmural full thickness biopsy specimens were obtained from each zone for electron microscopy before, and 1 and 4 hours after occlusion. Endocardial and epicardial layers were also obtained for assessment of myocardial potassium ion (K+) and sodium ion (Na+) concentrations. Before coronary occlusion, local Q waves were recorded an average depth of 1.0 +/- 0.34 mm from the endocardial surface. After 1 hour of occlusion, Q waves appeared at an average depth of 3.8 +/- 0.67 mm and progressed to a depth of 5.2 +/- 0.7 mm at 2 hours, 6.2 +/- 0.5 mm at 3 hours and 7.0 +/- 0.5 mm at 4 hours. After 1 hour, ultrastructural changes of early ischemia, including a decrease in glycogen and mild mitochondrial swelling, were seen in the endocardial layer; the epicardial layer showed normal morphologic features. After 4 hours, the endocardial layer showed well developed ischemic changes marked by the loss of mitochondrial cristae, vacuolization, the appearance of amorhopous mitochondrial cristae, vacuolization, the appearance of amorphous mitochondrial densities, an increase in interfibrillary space and the appearance of I bands. In contrast, the epicardial layer at this time showed only early ischemic changes. At the end of 4 hours, the endocardial layer showed a marked decrease in myocardial K+ concentration and an increase in Na+ concentration leading to complete reversal of K+/Na+ ratio (0.7 +/- 1.0; P less than 0.001). In the epicardial layer, a smaller decrease in K+ concentration and an increase in Na+ concentration occurred, resulting in a diminution but not a reversal of K+/Na+ ratio (1.4 +/- 0.2; P less than 0.005). Thus, the dynamic evolution of an acute myocardal infarction involves a sequential progression from endocardium to epicardium as a function of time, resulting in an epicardial "border zone" in the early stages after acute coronary occlusion.
Am J Cardiol 1978 Sep
PMID:Progressive transmural electrographic, myocardial potassium ion/sodium ion ratio and ultrastructural changes as a function of time after acute coronary occlusion. 68 53

The effect of lidocaine on His-Purkinje conduction in dogs with ischemic damage to the His bundle was compared with the effect of lidocaine in normal dogs. The anterior septal artery was ligated in 14 dogs, and 30 minutes later atrial pacing was performed to increase residual ischemic damage. Four to 6 days later, His bundle recordings were obtained during sinus rhythm and atrial pacing before and after the administration of lidocaine in a dose of 2 mg/kg and a total dose of 4 mg/kg. His bundle recordings were also obtained in nine control animals beofre and after the administration of lidocaine. Lidocaine significantly increased the H-V time in the animals with ischemic damage during sinus rhythm and at all packing rates. It also resulted in advanced His-Purkinje conduction defects including His bundle block and right bundle branch block in these animals. In contrast, the effect of lidocaine in the normal animals was negligible. It is concluded that lidocaine significantly depresses His-Purkinje conduction in the setting of preexisting ischemic damage. These results suggest that lidocaine may be used as a diagnostic tool to unmask latent His-Purkinje conduction defects due to ischemia.
Am J Cardiol 1978 Oct
PMID:Effect of lidocaine on conduction in the ischemic His-Purkinje system of dogs. 69 42


<< Previous 1 2 3 4 5 6 7 8 9 10 Next >>