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Query: UMLS:C0022116 (ischemia)
 91,303 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Myocardial ischemia results when halothane is administered to animals with severe coronary stenosis. This study was done to separate the effect of halothane, per se, on myocardial ischemia from indirect cardiovascular effects, primarily hypotension, that might cause ischemia by altering the oxygen supply-demand balance. Eight dogs underwent sterile surgery for implantation of sonomicrometer crystals and atrioventricular (A-V) heart block. One week later, each dog was anesthetized with morphine and chloralose. Heart rate was controlled by ventricular pacing and altered in five steps from 50 to 150 beats/min. Arterial blood pressure was controlled by blood withdrawal or phenylephrine infusion at four levels of arterial pressure (60 to 120 mmHg). Regional myocardial contraction was measured at each of the resulting 20 points as an indicator of myocardial ischemia. Twenty points were collected under each of four conditions in each animal: control, halothane (1% inspired), stenosis, halothane plus stenosis. Systolic thickening in the presence of stenosis was divided, on a point-by-point basis, by values obtained in the absence of stenosis to obviate the direct effects of blood pressure and heart rate on thickening. A separate normalization was done for data obtained in the presence of halothane. The normalized data demonstrate impaired systolic contraction at low arterial pressures and high heart rates. Multiple regression analysis failed to demonstrate a significant effect of halothane on systolic contraction once the effects of blood pressure, heart rate, and the negative inotropic effect of halothane were taken into account. Thus, the contraction failure that occurred during halothane and severe stenosis was mediated by changes in hemodynamics.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Impaired systolic thickening associated with halothane in the presence of a coronary stenosis is mediated by changes in hemodynamics. 396 80

Two patients with complete heart block complicating extensive anterior myocardial infarction underwent late (greater than 40 hours) coronary reperfusion with angioplasty. One to one atrioventricular conduction was restored within minutes of reperfusion despite a lack of measurable ventricular muscle salvage as demonstrated by ventriculography 1 week later. The evidence favors reversible ischemia rather than extensive necrosis of the proximal conduction system as the mechanism of heart block in this subgroup of patients.
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PMID:Effects of reperfusion on complete heart block complicating anterior myocardial infarction. 623 90

The term coronary artery spasm should not be used interchangeably with the specific clinical syndrome "variant angina" since it does occur in other acute and chronic ischemic heart disease syndromes. The term coronary artery spasm should not be applied to patients with ischemic heart disease unless there is clinical, angiographic, and physiologic evidence of its presence. The diagnosis of coronary artery spasm is confirmed by angiography, i.e. change in caliber of the coronary arteries plus evidence of ischemia. Probable diagnosis is in patients who have the syndrome of variant angina, i.e. rest angina associated with ST segment elevation on the electrocardiogram. One can be highly suspicious that the spasm is at work in patients who have rest angina, especially those with unstable angina. One can be suspicious of patients who have variable effort angina or walk-through angina. Coronary artery spasm is a possibility in patients with an acute myocardial infarction or acute re-infarction and is also possible that sudden death in patients with normal coronary arteries can be related to coronary artery spasm. Coronary artery spasm is the usual cause of myocardial ischemia in patients with rest angina without effort angina. This has also commonly been documented in patients with rest and effort angina. There are isolated reports suggesting that patients with effort angina pectoris also develop coronary artery spasm. Coronary artery spasm has been documented to occur in association with acute myocardial infarction. Whether coronary artery spasm is the cause or the result of myocardial infarction has not been determined at this time. However, the recent combined use of intracoronary nitroglycerin and intracoronary streptokinase in patients with acute myocardial infarction has shown reversal of totally obstructed arteries and suggests the relationship between coronary artery disease, coronary artery spasm, and in situ coronary thrombosis. The incidence of sudden death in patients with documented coronary artery spasm is unknown. But, since complete heart block and/or ventricular tachycardia occur during episodes of coronary artery spasm, it is not unreasonable to assume that some patients have died as a result of these rhythm disturbances. The prognosis of patients with coronary artery spasm seems to depend on the presence or absence of severe coronary atherosclerosis, i.e. those with severe disease have a worse prognosis. Current therapy of patients with coronary artery spasm involves the use of nitrates and calcium antagonists.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Role of coronary artery spasm in ischemic heart disease. Therapeutic implications. 633 45

A 62-year-old man who was under observation following an episode of severe chest pain developed complete heart block and hypotension after receiving sublingual nitroglycerin. The reaction occurred while the patient was receiving an intravenous maintenance infusion of lidocaine but did not occur in response to either nitroglycerin alone or lidocaine alone. There was no evidence of acute cardiac ischemia nor of clinically significant underlying heart disease. Complete heart block after sublingual nitroglycerin in the absence of significant cardiac disease is an exceedingly rare phenomenon.
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PMID:Complete heart block after sublingual nitroglycerin. 640 6

Leukotriene D4 (1--20 micrograms/kg i.a.) administered to conscious spontaneously hypertensive rats (SHR) and WKY rats caused acute elevation of blood pressure in both groups, but only in SHR a prolonged hypotensive period followed the hypertensive event. SHR rats had tachycardia during the hypertensive phase and relative bradycardia during the hypotensive phase which was more pronounced and prolonged than in WKY rats. In SHR rats only, plasma epinephrine and norepinephrine were elevated (6- and 3-fold, respectively) at the peak of the hypertensive period. Pretreatment of SHR rats with indomethacin (5 mg/kg) potentiated the LTD4-induced pressor response and shortened the hypotensive-bradycardic effect of LTD4. This same biphasic, dose-dependent response to LTD4 (1--20 micrograms/kg i.v.) was present in pithed SHR rats. Therefore, a direct action of LTD4 on vascular smooth muscle and heart is suggested. In all WKY rats and some SHR rats, a bradycardic effect of LTD4 resulted from sinus bradycardia, whereas in pithed SHR rats impaired conduction varying from transient second degree atrioventricular block to complete heart block was observed. Electrocardiographic signs of ischemia were seen only in LTD4-injected, pithed SHR rats. These results suggest fundamental differences between SHR and WKY rats in regard to their sensitivity to lipoxygenase products.
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PMID:Leukotriene D4: cardiovascular and sympathetic effects in spontaneously hypertensive rats (SHR) and Wistar-Kyoto (WKY) rats. 689 89

The effects of separate increases in atrial and ventricular contraction rates on the distribution of coronary flow within the heart were determined in conscious dogs with chronic heart block. Atrial tachycardia increased atrial blood flow and did not change ventricular blood flow. Ventricular tachycardia increased ventricular blood flow but not atrial blood flow. The results are consistent with the concept of local regulation of coronary perfusion by local myocardial energy turnover. The results also call attention to a potential adverse impact of atrial tachyarrhythmia in patients with underlying coronary ischemia.
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PMID:Independent regulation of atrial coronary blood flow by atrial contraction rate in conscious dogs. 719 59

Chemotherapy drugs have been reported to cause cardiac side effects including cardiomyopathy, ischemia, arrhythmias, and myocardial necrosis. Most important in terms of daily practice is anthracycline-induced cardiomyopathy. The bisdioxopiperazine compound, dexrazoxane (ICRF-187, ADR-529), has been shown to prevent this cumulative side effect of the anthracyclines. Recent randomized trials performed in breast cancer and in pediatric sarcoma patients have demonstrated the efficacy of this approach, which permits the administration of anthracyclines to greater cumulative doses and thus leads to a substantial reduction in the incidence of decreased left-ventricular ejection fraction or congestive heart failure. Response rates were not significantly different with the use of dexrazoxane in these trials. The risk ratio for a cardiac event was decreased by two to threefold in randomized breast studies involving more than 700 women. Paclitaxel also has been reported to cause arrhythmias and possibly ischemia. In a large data base, National Cancer Institute investigators found a 0.29% incidence of grade 4 or 5 cardiac toxicities, including heart block, ventricular tachycardia, and ischemic events. Other important chemotherapy-related cardiac toxicities discussed include fluorouracil-induced angina and arrhythmias, interleukin-4 induced-cardiomyopathy, and cardiotoxicity associated with autologous bone marrow transplantation procedures.
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PMID:Cardiotoxicity and cardioprotection during chemotherapy. 757 76

Cardiac toxicity was first noted in patients receiving Taxol during continuous cardiac monitoring, which was performed because of the high incidence of serious hypersensitivity reactions noted early in phase I trials. After cardiac events were documented, patients with cardiac disease and those on medications known to alter cardiac conduction were excluded from most trials. The cardiac events reported with Taxol from the initiation of NCI-sponsored clinical trials through August 1992 are summarized. Adverse cardiac events were reviewed in four clinical databases: 1) the Cancer Therapy Evaluation Program's Adverse Drug Reaction database following treatment of more than 3400 patients; 2) all cardiac toxicities in patients on GOG-111 who were randomized to cisplatin plus either Taxol or cyclophosphamide; 3) cardiac toxicity in 198 patients who received 618 courses of Taxol with or without cisplatin during continuous cardiac monitoring; and 4) cardiac toxicities reported for the first 696 patients on NCI TRC-9103 for ovarian cancer. Published reports of studies of taxine's cardiac effects, and of cardiac toxicity associated with yew poisoning, Cremophor EL, and H1 and H2 antagonists, are also reviewed. In patients without significant cardiac risk factors, asymptomatic sinus bradycardia is frequent (approximately 30%). Heart block and conduction abnormalities occur infrequently and are often asymptomatic. The casual relationship of Taxol to atrial and ventricular arrhythmias and cardiac ischemia is less clear because many patients had other conditions known to be associated with cardiac events. Nevertheless, the incidence of serious cardiac events was low. Routine cardiac monitoring is not required for patients without risk factors. There are, however, insufficient data to make treatment recommendations for patients with cardiac disease and those taking medications that alter cardiac conduction. To maximize patient safety and the clinical database, physicians who administer Taxol should continue to be alert to potential cardiac toxicities associated with Taxol.
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PMID:A reassessment of cardiac toxicity associated with Taxol. 791 18

While the development of pharmacological cardioplegic solutions for myocardial protection during cardiopulmonary bypass (CPB) have significantly lengthened the safe operating time for cardiac surgical procedures, the introduction of hypothermic hyperkalemic cardioplegia (CPG) has markedly increased the incidence of postoperative arrhythmias and conduction abnormalities. Using a customized modification of a computerized mapping system, we have developed a large animal porcine model of CPB that is exquisitely sensitive to the electrophysiological (EP) derangements imposed by ischemia and cardiac arrest. This model is able to measure spatial and temporal parameters of ventricular activation with high resolution, using an array of up to 84 epicardial electrodes that can be reproducibly placed on the surface of the heart utilizing known epicardial anatomical markers (e.g., coronary arteries). With this system we have measured the spectrum of clinically observed EP disturbances caused by CPG, from slowed intraventricular conduction to complete heart block. Compared to the control group of hypothermia alone, 2 hours of crystalloid CPG arrest had a significant slowing effect on ventricular activation (p < 0.05). CPG was accompanied, in each animal, by profound changes in the spatial distribution of ventricular activation and persistent slowing of ventricular activation. Traditional EP parameters of effective refractory period and pacing threshold were unchanged by CPG. Smaller temporal and spatial changes were observed in the control group, but were always reversed by 90 minutes of warm reperfusion. We conclude that CPG induces injury of the specialized conducting system and, to a lesser degree, the myocardium. This model will afford us the opportunity to test new methods of CPG to further improve myocardial preservation during CPB.
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PMID:Electrophysiological consequences of hypothermic hyperkalemic elective cardiac arrest. 846 98

Central nervous system involvement in neonatal lupus erythematosus (NLE) has not been previously reported. We report four patients with NLE, all with complete congenital heart block and three with cerebral ultrasound and color Doppler flow imaging (CDFI) studies demonstrating evidence of associated vasculopathy in the gangliothalamic vasculature. CDFI confirmed blood flow through the affected vessels, indicating that blood flow was not compromised at this early stage. Short-term follow-up revealed no signs of progression of the vasculopathy, focal ischemia, gangliothalamic atrophy, or neurological impairment. Nevertheless, the implications of this finding with respect to the natural history of NLE remain to be defined, particularly in cases in which the disease develops into systemic lupus erythematosus later in life. Besides specific diagnostic studies for NLE, cerebral ultrasound, and CDFI studies are mandatory in all cases of complete congenital heart block, regardless of whether mothers are diagnosed as having connective-tissue disease or not. Neonates with signs of vasculopathy in the gangliothalamic region should be examined for NLE.
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PMID:Central nervous system vasculopathy in neonatal lupus erythematosus. 888 46


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