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)

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.
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PMID:Paroxysmal reciprocating sinus tachycardia. 59 Feb 95

The electrocardiogram was monitored in 51 patients during fiberoptic bronchoscopic procedures and was compared to recordings made before premedication. Sixteen of the patients had heart disease. During the bronchoscopic procedure, the heart rate increased by 154 "/- 5 percent (+/- SE). The frequency of atrial ectopic beats was minimally increased, by an average 0.15 +/- 0.12 beats per minute (not significant). Ventricular ectopic beats became less frequent during the bronchoscopic procedure (-0.17 +/- 0.41 beats per minute; not significant), and there was no ventricular tachycardia. Frequent ventricular ectopic beats were seen mainly during bronchoscopic procedures in patients with coronary heart disease, but even in this group, ventricular ectopic beats became less frequent than at rest (-1.13 +/- 1.46 beats per minute; not significant). The nearly uniform sinus tachycardia that was observed was well tolerated but could predispose coronary patients to ischemia; however, the fiberoptic bronchoscopic procedure per se does not enhance prior ectopy.
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PMID:Arrhythmias from fiberoptic bronchoscopy. 67 41

To investigate the potential myocardial ischemic effects of ritodrine, we studied 36 singleton and four twin preterm pregnancies during ritodrine therapy. We serially determined serum creatinine phosphokinase (CPK-MB fraction) and lactic dehydrogenase isoenzymes and performed electrocardiography before and during ritodrine infusion and again within the first 24 hours of oral drug therapy. We observed that serum CPK-MB and lactic dehydrogenase isoenzymes remained within the normal range during therapy periods. The incidence of sinus tachycardia and non-specific T wave changes were 100% and 25%, respectively. In three of four twin pregnancies, ST-T segment depression in leads I, V4, V5, and V6 of the electrocardiogram was noted. Our study suggests that (1) the recommended ritodrine regimen does not produce direct myocardial damage, and (2) ritodrine may cause cardiac ischemia as determined by electrocardiography, which theoretically would progress to myocardial damage if not treated properly.
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PMID:Cardiac isoenzymes and electrocardiographic changes during ritodrine tocolysis. 224 70

The effect of intravenous (IV) amiodarone (300 mg) on heart rate was investigated in 22 patients with acute myocardial infarction (18) or ischemia (4) and sinus tachycardia. There were 11 men and 11 women (age range, 48 to 83 years; mean, 63.5). Amiodarone IV slowed the mean heart rate from 109 +/- 14 beats/min to 94 +/- 15 beats/min (p less than 0.0005). There was a linear correlation between the initial heart rate (preamiodarone) and the final heart rate (postamiodarone), (r = 0.6930, p less than 0.0005). Most of the patients with initial heart rates higher than the mean maintained relatively high heart rates (above the mean), while most patients with lower initial heart rates showed low heart rates (below the mean) after amiodarone administration. Patients in Killip class 1 showed a significant reduction in heart rate after receiving amiodarone, from a mean of 105 +/- 10 to 88 +/- 11 beats/min (p less than 0.01). Patients in Killip class 2 also had reduced heart rates (118 +/- 14 to 81 +/- 39 beats/min), but these changes were not statistically significant. Of the three patients in Killip class 3 to 4, the heart rate slowed by 10 beats/min in one, while in the remaining two no changes were observed. There were no significant side effects from the administration of amiodarone.
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PMID:The effect of intravenous amiodarone on heart rate in patients with acute myocardial infarction or ischemia and sinus tachycardia. 340 40

Nineteen patients with syndrome X (typical exertional angina, positive exercise test response [at least 0.1 mV of ST-segment depression], no evidence of coronary spasm and angiographically normal coronary arteries) underwent continuous 48-hour electrocardiographic (ECG) monitoring during unrestricted daily life. Fifty-eight ischemic episodes of at least 0.1 mV of ST-segment depression were observed in the same ECG leads that showed ST depression during stress testing: 28 (48%) were accompanied by anginal pain and 30 (52%) were asymptomatic. No significant differences were found between painful and silent ST-segment depression with regard to the number of episodes, their temporal distribution, magnitude, duration or heart rate (HR) at onset of ST-segment depression. In the minute preceding ischemic ST shifts, HR did not change in 33% of episodes or increased by less than 10 beats/min in 28%. HR at onset of ST depression was significantly lower during ambulatory ECG monitoring than during exercise testing (98 +/- 18 vs 117 +/- 18 beats/min, p less than 0.01). During ambulatory monitoring, 85 episodes of sinus tachycardia (exceeding by 10 to 80 beats/min the HR that triggered ischemia during exercise testing) occurred in the absence of angina or ST-segment shifts. The results of this study suggest that in patients with syndrome X, myocardial ischemia frequently develops during daily life; silent ischemia is an important component of this syndrome; and increased oxygen demand in the presence of impaired coronary vasodilatory capacity is not the only cause of myocardial ischemia. Active mechanisms that transiently reduce coronary flow may act and explain occurrence of angina at rest and with minimal exertion.
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PMID:Transient myocardial ischemia during daily life in patients with syndrome X. 378 14

One hundred twelve patients in preterm labor were followed prospectively, with electrocardiograms taken before ritodrine therapy and at 6 and 24 hours of treatment. Ninety-six percent of patients developed sinus tachycardia. Other changes were seen in 79% of the study group. These changes included ST segment depression in 70%, T wave flattening or inversion in 55%, and prolongation of the QT interval in 35% of our sample. None of the electrocardiograms showed the presence of a significant axis deviation, a change in QRS interval, or arrhythmia. No correlation was seen between symptoms of ischemia and electrocardiographic changes. A drop in potassium concentration was noted initially, but a direct correlation between potassium concentrations and frequency of electrocardiographic changes was not present. We conclude that the electrocardiographic changes that are often observed during myocardial ischemia may be frequent in asymptomatic patients treated with ritodrine and that these changes may be a physiologic expression of ritodrine-induced tachycardia or hypokalemia. The validity of the use of the presence of electrocardiographic changes as the only criterion for discontinuation of ritodrine therapy is questioned.
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PMID:Electrocardiographic changes associated with ritodrine-induced maternal tachycardia and hypokalemia. 396 85

The role of beta-adrenergic receptor blockade in preventing ventricular fibrillation in a conscious canine model of sudden coronary death was examined using d,l-nadolol and the non-beta-adrenergic receptor blocking isomer, d-nadolol. On day 4, after a temporary 90-min occlusion of the left anterior descending coronary artery, an anodal current of 150 microA was applied to the intimal surface of the left circumflex coronary artery. Occlusive or nonocclusive thrombosis of the artery was accompanied by ST-segment changes. In saline-treated animals (n = 15), ST-segment changes were followed by sinus tachycardia and QT-segment prolongation, with development of ventricular premature beats. Ventricular fibrillation developed in 14 animals (93%). Pretreatment with 1 (n = 9) or 8 mg/kg d,l-nadolol (n = 13) did not alter the development of left circumflex coronary artery thrombosis and ischemic ST-segment changes, but decreased the incidence of ventricular fibrillation and increased survival at 24 h (56% and 63%, respectively) (p less than 0.01 versus saline). d,l-Nadolol also attenuated the sinus tachycardia and QT-interval prolongation accompanying acute ischemia. d-Nadolol (1 mg/kg), the non-beta-adrenergic receptor blocking isomer, failed to prevent development of ST-segment changes. Sinus tachycardia and QT-interval prolongation were not prevented, and ventricular fibrillation developed in all eight animals (100%). In animals without previously induced anterior myocardial ischemic injury (n = 10), left circumflex coronary artery thrombosis failed to produce sinus tachycardia and QT-interval prolongation and was associated with a lower incidence of ventricular fibrillation (20%, p less than 0.005).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Antifibrillatory actions of d,l-nadolol in a conscious canine model of sudden coronary death. 619 59

In this report, we evaluated the cardiac findings of 15 children with polyarteritis nodosa. The age range of the patients was 4-14 years; with a mean of 10 years. All have had systemic involvement of the disease. The most common findings in cardiac evaluation were diminished left ventricular systolic functions and mild mitral and/or tricuspid valve regurgitation. One patient had pericardial thickening with no effusion. One had sinus tachycardia. There were no signs of myocardial infarction or ischemia clinically or electro-cardiographically. In conclusion, we did not find cardiac complications, such as pericarditis or myocardial infarction, to be as frequent as in previous reports. However, even in asymptomatic patients, systolic dysfunction or valvular involvement were common findings in patients with polyarteritis nodosa, which were not reported previously. These findings may be due to the histological changes of the myocardium or atrioventricular valves. Although these were not severe and fatal lesions, long-term follow-up of these patients with echocardiography may help to determine the course of cardiac involvement.
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PMID:Cardiac involvement in childhood polyarteritis nodosa. 926 36

We present a case of prolonged myocardial ischemia in a young healthy male presenting for nasal polypectomy and tonsillectomy. Induction of anesthesia proceeded uneventfully. Immediately after surgical incision, the patient developed a sinus tachycardia with ST-segment depression in leads II and III, and ST elevation in leads aVR, aVL, aVF, and V. Depth of anesthesia was increased, esmolol was administered, which slowed the heart rate, and the procedure was terminated. However, myocardial ischemia only gradually resolved, leaving residual T-wave flattening in lead III by day 3 postoperatively. After extensive investigation to rule out other causes of ischemia, we considered cardiotoxicity due to intranasally administered cocaine with epinephrine to be the most likely precipitant. Nasal packing with gauze soaked in a solution containing cocaine 3 mg/kg and epinephrine 1 mg occurred just 40 minutes prior to induction of anesthesia. Topical intranasal cocaine is rapidly and reliably absorbed systemically, with peak plasma concentrations occurring within 30 to 60 minutes, corresponding to the time course of cocaine administration and surgical stimulation in this patient. Systemic absorption of topical intranasal cocaine has previously been reported to cause adverse cardiac sequelae, including myocardial infarction. This report reinforces the need for caution regarding the use of topical intranasal cocaine, particularly if used in combination with epinephrine.
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PMID:Prolonged perioperative myocardial ischemia in a young male: due to topical intranasal cocaine? 1052 15

Multisite pacing for the treatment of heart failure has added a new dimension to the electrocardiographic evaluation of device function. During left ventricular (LV) pacing from the appropriate site in the coronary venous system, a correctly positioned lead V1 registers a right bundle branch block pattern with few exceptions. During biventricular stimulation associated with right ventricular (RV) apical pacing, the QRS is often positive in lead V1. The frontal plane QRS axis is usually in the right superior quadrant and occasionally in the left superior quadrant. Barring incorrect placement of lead V1 (too high on the chest), lack of LV capture, LV lead displacement or marked latency (exit block or delay from the stimulation site), ventricular fusion with the spontaneous QRS complex, a negative QRS complex in lead V1 during biventricular pacing involving the RV apex probably reflects different activation of an heterogeneous biventricular substrate (ischemia, scar, His-Purkinje participation in view of the varying patterns of LV activation in spontaneous left bundle branch block) and does not necessarily indicate a poor (electrical or mechanical) contribution from LV stimulation. In this situation, it is imperative to rule out the presence of coronary venous pacing via the middle cardiac vein or even unintended placement of two leads in the RV. During biventricular pacing with the RV lead in the outflow tract, the paced QRS in lead V1 is often negative and the frontal plane paced QRS axis is often directed to the right inferior quadrant (right axis deviation). In patients with sinus rhythm and a relatively short PR interval, ventricular fusion with competing native conduction during biventricular pacing may cause misinterpretation of the ECG because narrowing of the paced QRS complex simulates appropriate biventricular capture. This represents a common pitfall in device follow-up. Elimination of ventricular fusion by shortening the AV delay, is often associated with clinical improvement. Anodal stimulation may complicate threshold testing and should not be misinterpreted as pacemaker malfunction. One must be cognizant of the various disturbances that can disrupt 1:1 atrial tracking and cause loss of ventricular resynchronization. (1) Upper rate response. The upper rate response of biventricular pacemakers differs from the traditional Wenckebach upper rate response of conventional antibradycardia pacemakers because heart failure patients generally do not have sinus bradycardia or AV junctional conduction delay. The programmed upper rate should be sufficiently fast to avoid loss of resynchronization in situations associated with sinus tachycardia. (2) Below the programmed upper rate. This may be caused by a variety of events (especially ventricular premature complexes and favored by the presence of first-degree AV block) that alter the timing of sensed and paced events. In such cases, atrial events become trapped into the postventricular atrial refractory period at atrial rates below the programmed upper rate in the presence of spontaneous AV conduction. Algorithms are available to restore resynchronization by automatic temporary abbreviation of the postventricular atrial refractory period.
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PMID:Electrocardiographic follow-up of biventricular pacemakers. 1584 37


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