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 compared patients with variant angina (ST-segment elevation during pain) who had normal or near normal coronary arteriograms (Group 1) with 20 in whom variant angina occurred in the presence of obstructive coronary lesions (Group 2). A long history of nonexertional angina without angina of effort or previous infarction was the rule in Group 1, whereas recent-onset unstable angina preceded by effort angina and infarction predominated in Group 2 (P less than 0.001). Normal electrocardiograms at rest, with ischemic ST-segment elevation in the inferior leads, and ischemia-induced heart block and bradycardia, characterized Group 1, whereas abnormal electrocardiograms, ischemic involvement or fibrillation were more common in Group 2 (P less than 0.001). Variant angina with normal coronary arteriogram generally has a benign course and is probably unrelated to atherosclerosis.
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PMID:Clinical syndrome of variant angina with normal coronary arteriogram. 98 80

A relationship of coronary arterial spasm to variant angina pectoris, subendocardial ischemia, major ventricular arrhythmias and myocardial infarction has been demonstrated. In 29 patients, spasm was angiographically observed in normal-appearing coronary arteries (7 patients) as well as superimposed on various degrees of coronary atherosclerotic obstruction (22 patients). All patients experienced an atypical anginal syndrome;16 patients also experienced typical exertional angina. Coronary spasm appeared to be a major contributory factor in eight occurrences of myocardial infarction and in 11 incidents of ventricular tachycardia, ventricular fibrillation and heart block. Coronary spasm in the 29 cases was distributed in the following fashion: left main trunk, 6 cases; right main trunk, 12 cases; proximal left anterior descending artery, 13 cases; proximal circumflex artery, 1 case; distal left anterior descending artery, 1 case; and distal circumflex artery, 2 cases. In 5 cases coronary spasm was noted at multiple sites.
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PMID:Spectrum of coronary arterial spasm. Clinical, angiographic and myocardial metabolic experience in 29 cases. 99 29

In an attempt to identify a group of blunt trauma victims with asymptomatic myocardial contusion (MC) who do not benefit from intensive cardiac monitoring, we prospectively divided 336 patients admitted to the SICU with possible MC following blunt trauma in the 6 years prior to January 1990 into three groups: Group 1 (n = 155, age 30.5 +/- 9 years) consisted of those patients admitted for mechanism of injury, J-point elevation, with or without minor chest injury. None developed arrhythmias. Their SICU length of stay (LOS) was 2.41 +/- 0.77 days. Group 2 (n = 43, age 31.5 +/- 10 years) patients had the same admission criteria as the patients in group 1 plus an abnormal emergency department ECG, i.e., arrhythmia, heart block, ischemia. None had cardiac complications. Their SICU LOS was 2.47 +/- 0.94 days. Group 3 (n = 138, age 40 +/- 20 years) patients had four or more rib fxs, a pulmonary contusion, a flail chest, or extra-thoracic injuries or were greater than 60 years of age. All required SICU admission for their non-cardiac injuries. Nineteen patients had cardiac complications requiring treatment. None had a cardiac death. Their SICU LOS was 10 +/- 22 days. We conclude that young patients with minor blunt thoracic trauma and a normal or minimally abnormal ECG do not benefit from cardiac monitoring.
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PMID:The clinical significance of myocardial contusion. 163 8

A 62-year-old woman was noted to have complete heart block immediately following an exercise stress test. Coronary arteriography subsequently revealed a significant lesion in the right coronary artery, which was successfully dilated. Thallium-exercise testing following angioplasty showed no evidence of inducible ischemia and no arrhythmia was seen, supporting the idea that exercise-related heart block may occur secondary to myocardial ischemia.
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PMID:Exercise-related atrioventricular block. Influence of myocardial ischemia. 195 24

Electrophysiologic disorders are common at all stages of heart failure due to myocardial mechanical factors, neuroendocrine disturbances, electrolyte abnormalities, or ischemia, and also because of cardiovascular drugs. The prevalence of various forms of heart block, bradycardias, and arrhythmias in heart failure is largely unknown, as is their relationship to the etiology of the syndrome. Complex and multiform ventricular premature beats and nonsustained ventricular tachycardia are common, and their frequency is broadly related to the severity of heart failure. Supraventricular arrhythmias are also common features of the syndrome. The heart failure syndrome has an ominous prognosis. Approximately half the patients die suddenly, but the causal relationship between preexisting arrhythmias and sudden death is not known. Equally vital is knowledge of the influence of drug therapy on the arrhythmias of heart failure, but at present this is scarce and needs further study.
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PMID:Arrhythmias in heart failure--therapeutic challenges. 204 70

To return to the patient's syncopal episode, it is clearer now that he probably did have a vasovagal reaction. An hour had elapsed since administration of morphine, making that etiology unlikely. The patient showed no evidence of heart block or acute ischemia. While nitrate induced hypotension may have contributed to his faint, that would not have explained his bradycardia. Worth noting is the fact that he developed nausea and lost consciousness as an arterial puncture was about to be performed. Had he been asked, the patient might have recalled other incidents of vasovagal fainting. A combination of factors may cause a brief syncopal episode in the ICU. Sorting out the causes of vasovagal syncope may be difficult if not impossible, and a syncopal episode may set a chain of events into motion that further complicates the situation. The patient with an acute, especially inferior MI who received intravenous medications is particularly prone to vagal-like reactions. Patients with nausea or extreme anxiety should be watched carefully and their symptoms treated.
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PMID:Vasovagal syncope. 280 52

In the critical period during which ischemia progresses to infarction, beta-blocking drugs are known to reduce oxygen demand and prevalence of arrhythmia. To investigate whether this treatment confers clinical benefits, 28 trials have been conducted involving some 27,500 patients during the early hours after onset of symptoms suggesting acute myocardial infarction (MI). Patients were randomized to receive either initial intravenous beta blocker plus oral maintenance or standard therapy. In toto, these trials indicated that early-intervention short-term beta-blocker treatment reduces: (1) the risk for early death, reinfarction, and ventricular fibrillation by about 15%; (2) enzymatic indices of infarct size; (3) the number of patients with threatened MI in whom a confirmed MI develops; and (4) the frequency of repetitive and nonrepetitive ventricular arrhythmias. Overall, the treated group had few major side effects other than a small excess of reversible and nonfatal heart block and hypotension. Retrospective analyses suggest (but do not prove) that the reduction in mortality is greatest for those treated within two hours of pain and during the first two days. These results indicate that early initial administration of intravenous beta blocker plus one week's oral beta-blocker treatment produces modest benefits that would presumably be of major public health importance if such treatment were widely used.
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PMID:Early intravenous beta blockade in acute myocardial infarction. 289 66

The effect of verapamil cardioplegia on atrioventricular conduction was examined in 19 dogs. During 90 minutes of ischemic arrest, five dogs received multidose potassium cardioplegia, containing 1.2 mg/L of verapamil (group 1), five received potassium cardioplegia containing 600 micrograms/L of verapamil (group 2) and nine animals received cardioplegia containing 300 micrograms/L of verapamil (group 3). Atrioventricular conduction was measured in all groups before bypass, after 90 minutes of ischemia and after 45 minutes of reperfusion. Specially designed plunge electrodes were used to monitor the electrical status of the heart during arrest in group 3 and, in addition, left ventricular function and concentration of high-energy phosphates were determined before and after ischemic arrest. Conduction was prolonged in four group 1 dogs and in two group 2. Atrioventricular conduction was measured in six group 3 dogs; five had prolonged conduction and one experienced second-degree heart block. Small-amplitude electrical potentials were recorded from the myocardium in two of nine dogs in group 3. Persistent electrical activity was associated with continued use of high-energy phosphates and resulted in decreased left ventricular function after 90 minutes of ischemic arrest. Our data indicate that small doses of verapamil will delay atrioventricular conduction and will not prevent small-amplitude electrical activity.
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PMID:Effect of various low-dose concentrations of verapamil cardioplegia on small-amplitude electrical activity during cardioplegic arrest. 333 75

Calcium channel blockers may prevent myocardial injury during cardioplegia and reperfusion. A prospective, randomized trial was instituted to evaluate the hemodynamic and myocardial metabolic recovery in 40 patients undergoing elective aorta-coronary bypass with either diltiazem in crystalloid potassium cardioplegia (n = 20) or crystalloid potassium cardioplegia (n = 20). In a preliminary trial, doses between 150 and 250 micrograms/kg reduced the period of heart block after cross-clamp removal (90 +/- 110 minutes) from that found with higher doses and improved myocardial metabolism. In the randomized trial, diltiazem cardioplegia (150 micrograms/kg) produced coronary vasodilatation during cardioplegia and produced less reactive hyperemia during reperfusion. Myocardial oxygen extraction was lower and myocardial lactate production was less after diltiazem cardioplegia during reperfusion. Tissue adenosine triphosphate and creatine phosphate concentrations were preserved better after diltiazem cardioplegia. The postoperative creatine kinase MB levels were less (p less than 0.05) after diltiazem cardioplegia, which indicated less myocardial injury. Postoperative volume loading demonstrated that systolic function (the relation between systolic blood pressure and end-systolic volume index) was depressed after diltiazem cardioplegia compared to crystalloid cardioplegia, but cardiac index was higher because afterload (mean arterial pressure) was lower and preload (end-diastolic volume index) was higher. Diltiazem cardioplegia preserved high-energy phosphates, improved postoperative myocardial metabolism, and reduced ischemic injury after elective coronary bypass. However, diltiazem was a potent negative inotrope and produced prolonged periods of electromechanical arrest. Diltiazem cardioplegia may be of value in patients with severe ischemia but should be used with caution in patients with ventricular dysfunction, and a dose-response relation must be established at each institution before clinical use.
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PMID:Diltiazem cardioplegia. A balance of risk and benefit. 351 6

We evaluated the initial electrocardiogram as a predictor of complications in 469 patients with suspected acute myocardial infarction. An electrocardiogram was classified as positive if it showed one or more of the following: evidence of infarction, ischemia, or strain; left ventricular hypertrophy; left bundle-branch block; or paced rhythm. Forty-two (14 per cent) of 302 patients with positive electrocardiograms had at least one life-threatening complication (ventricular fibrillation, sustained ventricular tachycardia, or heart block), as compared with 1 (0.6 per cent) of 167 patients with a negative electrocardiogram. Life-threatening complications were therefore 23 times more likely if the initial electrocardiogram was positive (P less than 0.001). Other complications were 3 to 10 times more likely (P less than 0.01), interventions were 4 to 10 times more likely (P less than 0.05), and death was 17 times more likely (P less than 0.001) in patients with a positive electrocardiogram. We conclude that patients with a negative initial electrocardiogram have a low likelihood of complications and could be admitted to an intermediate care unit instead of a coronary care unit. This would reduce admissions to the coronary care unit by 36 per cent and thereby save considerable hospital costs without compromising patient care.
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PMID:Use of the initial electrocardiogram to predict in-hospital complications of acute myocardial infarction. 392 May 20


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