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Query: UMLS:C0151744 (myocardial ischemia)
 31,282 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Analgesic abuse is a major public health hazard in Australia, and analgesic nephropathy with consequent terminal renal failure is the underlying cause in 20% of the patients requiring dialysis and transplantation. Analgesics are invariably taken in the form of compounds and mixtures. In the aspirin-phenacetin-caffeine (APC) mixture, aspirin appears to be the major nephrotoxic agent and phenacetin appears to play a secondary and synergistic role. The renal disease associated with abuse of analgesics is characteristic and is part of a much wider clinical syndrome, the analgesic syndrome, which includes peptic ulcer disease (35%), anemia (60 to 90%), hypertension (15 to 70%), ischemic heart disease (35%), psychological and psychiatric manifestations, pigmentation, and possible gonadal- and pregnancy-related effects. The primary lesion in analgesic nephropathy is renal papillary necrosis (RPN), and this is a nephrotoxic effect common to all nonsteroid antiinflammatory agents. The most important factor in the management of patients with analgesic nephropathy is the cessation of analgesic abuse, and this leads to improvement and stabilization of renal function. A small proportion of patients will, however, deteriorate in relation to accelerated hypertension, persistent proteinuria, ischemic heart disease, and complications leading to nephrectomy. Patients with analgesic nephropathy are poor risk patients and have a poor prognosis, even after dialysis and transplantation.
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PMID:Analgesic nephropathy: etiology, clinical syndrome, and clinicopathologic correlations in Australia. 36 34

The influence of a 6-week intervention on factors thought to be related to ectopic cardiac rhythms was tested in normal men with frequent ventricular premature contractions (VPCs), using a randomized, controlled and partial crossover design. The VPC intervention trial experimental regimen included total abstinence from caffeine and smoking, reduction of alcohol intake, and a physical conditioning program. Effects were studied in detail among 81 healthy men with persistent VPCs. VPCs were measured during standard states of rest, dynamic and isometric exercise and other stresses, and 24-hour ambulatory monitoring. Adherence to the treatment was excellent. The experimental group achieved more than 80% of activities asked of them, and little "contamination" occurred in the control group. VPCs were analyzed according to VPC/min, VPC/man and VPC/total number of heart beats. Moderate changes in VPC rates occurred in both experimental and control groups but no significant group differences were found at rest or during any induction test. This 6-week, multiple-factor "hygienic" intervention program had no significant influence on the frequency or occurrence of VPCs in apparently normal men with persistent and frequent VPCs. Because the mechanisms and the significance of VPCs are different in patients with ischemic heart disease, our approach and methods may be useful for similar trials among cardiac patients of adjunct or non-drug therapy for ectopic rhythms.
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PMID:Ventricular premature contractions: a randomized non-drug intervention trial in normal men. 42 17

The morphological analysis of the portions of the interventricular septum and left ventricular wall in cats has revealed dystrophic and necrotic changes in the myocardium after administration of caffeine followed by adrenaline: haemorrhages, intravascular thrombogenesis, dystrophic and necrobiotic changes in myocytes. In early periods of acute ischemic heart disease morphine, fibrinolysin, heparin and Inosie F either abolished (fibrinolysin) or considerably decreased (heparin and Inosie F) a tendency toward intravascular thrombogenesis and damage to the myocardial parenchyma.
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PMID:[Effect of agents used in the therapy of acute ischemic heart disease on the histomorphological changes in the myocardium in acute dystrophy]. 47 57

The effect of caffeine on heart rate, blood pressure, and cardiac rhythm has long been a controversial issue. A review of the literature reveals numerous articles evaluating the effects of caffeine on normal subjects, fewer evaluating the effects of caffeine on patients with cardiac disease and patients after myocardial infarction. Although the findings for the various populations have been inconsistent, recent studies with large cohorts have clarified the issue. Moderate consumption of caffeine does not significantly increase the risk of a coronary event nor increase the frequency of cardiac arrhythmias. This conclusion applies to healthy persons, patients with ischemic heart disease, and those with serious ventricular ectopy. Patients with cardiac disease should be allowed to consume four to five cups of caffeinated beverages per day while in the coronary care unit or progressive care unit under the surveillance of nursing staff.
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PMID:Coronary precautions: should caffeine be restricted in patients after myocardial infarction? 162 6

The effect of high dose caffeine on ventricular arrhythmias was examined in 35 patients with recent myocardial infarctions. All patients received caffeine 450 mg or placebo on separate days using a randomized double-blind study design. Continuous Holter electrocardiographic recordings were performed for 8 h. Caffeine ingestion did not cause any increase in the frequency or complexity of ventricular ectopy with 19 of 35 patients experiencing ventricular arrhythmias after caffeine compared with 24 of 35 with placebo. Serious ventricular ectopic activity (including ventricular couplets and tachycardia) was similar on both study days. Moderately high doses of caffeine do not appear to increase ventricular arrhythmias in this patient population with ischemic heart disease.
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PMID:High dose caffeine and ventricular arrhythmias. 234 Apr 43

Alternans in heart is important as pulsus alternans in cardiac failure and electrophysiological alternans in myocardial ischemia. The explanation of this phenomenon is still unclear. We attempted to investigate the cellular mechanisms of alternans by measuring intracellular free calcium concentration [( Ca2+]i) with the photoprotein aequorin in isolated ferret papillary muscles. Tension and length were also recorded simultaneously. Transient mechanical alternans lasting five to 20 contractions could be reliably induced in this preparation by following a 30-second rest period with stimulation at a fast rate (2-4 Hz). Production of sustained mechanical alternans, which lasted longer than 20 contractions and could persist for several hundred contractions, required additional interventions, consisting of a lower temperature (25 degrees C), a lower external calcium concentration (1 mM), and a lower pH (6.91) than control conditions (0.33-0.5 Hz, 30 degrees C, 2 mM Ca2+, pH 7.36). Transient mechanical alternans was associated with transient in-phase alternation of aequorin light and, hence, [Ca2+]i. Sustained mechanical alternans was associated with sustained in-phase alternation of aequorin light as well as incomplete relaxation of tension. However, when muscles were switched from isometric to unloaded isotonic contraction, relaxation between stimuli was complete but contraction and the aequorin light signal continued to alternate. The addition of 10 mM caffeine or 10 microns ryanodine abolished transient and sustained mechanical alternans and also abolished the associated alternation of aequorin light. Commensurate with the action of ryanodine, which allows the sarcoplasmic reticulum to reaccumulate calcium to a limited extent after a period of rapid stimulation, sustained mechanical alternans sometimes reappeared in an attenuated form 30 to 50 contractions after the addition of ryanodine. These results demonstrate that incomplete muscle relaxation between beats need not be present for alternans to occur, and support the hypothesis that alternans is caused by intracellular calcium cycling involving the sarcoplasmic reticulum.
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PMID:Changes in intracellular calcium during mechanical alternans in isolated ferret ventricular muscle. 230

We evaluated the effect of caffeine on ventricular ectopic activity in a group of 50 consecutive patients with malignant ventricular arrhythmia. The clinical arrhythmia in these patients (mean age, 61 years) was recurrent ventricular tachycardia in 21 (42%), ventricular fibrillation in three (6%), and symptomatic nonsustained ventricular tachycardia in 26 (52%). Forty-two (84%) had either ischemic heart disease or cardiomyopathy. Each patient underwent two short-term drug trials on successive days, receiving either decaffeinated coffee mixed with 200 mg of caffeine or the decaffeinated drink alone. Continuous electrocardiographic recordings were made during the 30-minute control period, the three-hour observation period, and the hourly bicycle exercise tests. Forty-five patients (90%) exhibited ventricular couplets and 29 patients (58%) had salvos of ventricular tachycardia during the testing. However, no differences between the caffeine and decaffeinated trials were observed in either individual or group data on total or repetitive ventricular arrhythmia. Serum catecholamine levels reflected the average increase in serum caffeine level but were not associated with enhanced arrhythmia. We found no evidence that a modest dose of caffeine is arrhythmogenic, even among patients with known life-threatening arrhythmia.
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PMID:The effect of caffeine on ventricular ectopic activity in patients with malignant ventricular arrhythmia. 246 48

It is generally agreed that a high release of noradrenaline in the heart may elicit cardiac arrhythmia. Furthermore, administration of aminophylline to patients with ischaemic heart disease frequently elicits ventricular premature beats and ventricular tachycardia. Recent data from animal experiments demonstrate that methylxanthines (aminophylline, caffeine, theophylline) can facilitate noradrenaline release from sympathetic nerve endings. Such facilitation of transmitter release is amplified when myocardial oxygenation is impaired, stressing its clinical significance in relation to ischaemic heart disease. If a similar amplification is also operative in man, a dose of methylxanthine causing a very modest increase in myocardial sympathetic transmitter release in the heart of a healthy subject may be sufficient to cause a three- to six-fold elevation in the local myocardial concentration of noradrenaline in a patient with ischaemic heart disease. We hypothesize that such hypoxia-induced facilitation of sympathetic transmitter release lies behind the reported connection between cardiac events and methylxanthines, for instance sudden cardiac death following coffee consumption.
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PMID:Coffee, catecholamines and cardiac arrhythmia. 274 38

The mechanism of action of coronary vasodilation after dipyridamole may be based on inhibition of cellular uptake of circulating endogenous adenosine. Since caffeine has been reported to be a competitive antagonist of adenosine we studied the effect of caffeine on the outcome of dipiridamole-201Tl cardiac imaging in one patient. During caffeine abstinence dipyridamole induced myocardial ischemia with down-slope ST depressions on the ECG, and reversible perfusion defects on the scintigrams. When the test was repeated 1 wk later on similar conditions, but now shortly after infusion of caffeine (4 mg/kg), the ECG showed no, and the scintigrams only slight signs of ischemia. We conclude that when caffeine abstinence is not sufficient, the widespread use of coffee and related products may be responsible for false-negative findings in dipyridamole-201Tl cardiac imaging.
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PMID:Caffeine reduces dipyridamole-induced myocardial ischemia. 279 13

This study investigates the possible role of oscillatory release of calcium from sarcoplasmic reticulum in the genesis of ventricular arrhythmias during acute myocardial ischemia and reperfusion in isolated rat hearts. We used ryanodine and caffeine, which are known to modulate the oscillatory release of calcium from sarcoplasmic reticulum. During 30 minutes of left main coronary artery ligation, all 13 control hearts developed ventricular premature beats (number of beats, 225 +/- 51) and ventricular tachycardia (duration, 123 +/- 21 seconds); five hearts developed ventricular fibrillation. In a separate series of experiments, reperfusion after 15 minutes of coronary artery ligation caused ventricular fibrillation to occur within 15 seconds in all 12 hearts. Ryanodine (10(-9) to 10(-7) M) abolished ventricular arrhythmias during coronary artery ligation and prevented reperfusion ventricular fibrillation. Ryanodine (10(-9), 10(-8), and 10(-7) M) caused 15%, 23%, and 74% decreases in the maximal rate of rise of left ventricular pressure development and 20%, 32%, and 85% decreases in the maximal rate of fall of left ventricular pressure development, respectively, prior to coronary artery ligation. During acute myocardial ischemia, ryanodine 10(-9) M maintained and 10(-8) M impaired left ventricular function; 10(-7) M caused left ventricular failure. Coronary perfusion rate did not increase during ischemia. Antiarrhythmic activity occurred independent of preservation of high energy phosphates, reduction in tissue lactate, or tissue cyclic adenosine monophosphate in the ischemic myocardium. Caffeine 10(2) M decreased the incidence of ventricular arrhythmias during ischemia and upon reperfusion; protection occurred coincident with development of diastolic contracture. Caffeine increased ischemic tissue cyclic adenosine monophosphate content and worsened tissue energy status.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Ryanodine and caffeine prevent ventricular arrhythmias during acute myocardial ischemia and reperfusion in rat heart. 282 12


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