Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0151744 (myocardial ischemia)
 31,282 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

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

Segmental reductions in blood flow together with segmental shifts in substrate metabolism from oxidation of fatty acids to aerobic and anaerobic usage of glucose, commonly associated with regional myocardial ischemia in humans, can now be assessed noninvasively with position emission tomography (PET). Characterization of metabolic rather than blood flow changes is superior for assessing tissue viability. Persistence of metabolic activity, though abnormal, in myocardial segments with reduced blood flow and function as detected by PET is associated with greater morbidity in patients post myocardial infarction and identifies in chronic ischemic heart disease injured but viable myocardium that benefits from surgical revascularization. PET also detects persistent metabolic activity in acutely infarcted tissue and hence may guide interventions for salvaging injured myocardium.
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PMID:Myocardial blood flow and metabolism in humans. 633 22

The judgment of the function of the left ventricle is computer-tomographically possible using the ECG-regulated cardio-computer-tomography in a temporary resolution of about 0.1 sec. The qualitative and quantitative evaluation of the systolic and diastolic changes of the ventricle in patients with normal CT-findings, with idiopathic hypertrophic subaortic stenosis and with disturbances of motility in chronic ischaemic heart disease confirms the possible functional evidence known from literature. The quantitative parameters, in particular the systolic abbreviation of the axis, allow an estimation of the motility. The measurement of the thickness at the interventricular septum and at the lateral wall of the myocardium as well as the systolic abbreviation of the axis and the left-ventricular ejection fraction are essentially higher in the idiopathic hypertrophic subaortic stenosis than in the normal group. The values of the patients with disturbances of motility in the ischaemic heart disease were clearly below. The diagnosis of the idiopathic hypertrophic subaortic stenosis with response of the size of obstruction by the telesystolic and telediastolic pictures is possible in a high percentage. Sequelae of the chronic ischaemic heart disease, e.g. scars, become visible by a narrowing or an absence of the normal edge of the myocardium. Global and localized disturbances of motility are diagnosable by phase-referred systolic and diastolic ECG-regulated pictures.
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PMID:[Computer tomographic evaluation of left ventricular kinetics]. 653 35

Arrhythmias may be controlled in most patients with recurrent supraventricular tachycardia or atrial fibrillation with small to moderate maintenance doses of amiodarone (100 to 400 mg/day). Moderate doses (400 mg/day) are also highly effective in suppressing "warning" ventricular arrhythmias in patients with chronic ischemic heart disease, particularly if the goal of treatment is to eliminate ventricular couplets, runs of ventricular tachycardia (VT), and the "R on T" phenomenon. Treatment and prevention of sustained recurrent VT and the malignant arrhythmias of chagasic myocarditis require, however, doses of about 800 mg/day, which may be higher than those needed for ischemic heart disease complicated by VT and ventricular fibrillation. Clinical studies suggest an elimination half-life for amiodarone of about 30 days (range 15 to 100 days). Thus there is a pretherapeutic latency period that varies according to the type of arrhythmia and the doses employed. The maximal effects (as well as the most significant adverse effects) are not attained before 90 to 150 days of treatment, and the antiarrhythmic protection may persist for varying intervals, up to 150 days or more, after the drug has been discontinued. Side effects are not negligible but are generally dose dependent. Despite these side effects, many patients have been treated by us with amiodarone for as long as 5 to 8 years--and for up to 10 years in some cases. Amiodarone appears to be one of the most promising drugs for the possible prevention of ventricular fibrillation and sudden death.
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PMID:Ten years of experience with amiodarone. 661 43

The effect of dobutamine on exercise performance was assessed in 20 patients with ischemic heart disease (CAD) and a positive stress test. These patients had a wide range of resting left ventricular ejection fraction (range 22% to 69%, mean 42%). Each patient entered a double-blind crossover study in which two identical exercise radionuclide ventriculograms were performed in patients on dobutamine, 5 micrograms/kg/min intravenously, or placebo. Dobutamine increased resting left ventricular ejection fraction. Although ejection fraction fell with dobutamine during submaximal exercise, it remained higher than with placebo. At peak exercise, ejection fraction fell to the same level on dobutamine as with placebo. Dobutamine diminished exercise time and time to ischemia while peak pressure-rate product was unchanged. Four of 20 patients developed complex ventricular premature beats, all while on dobutamine. Although useful when administered to resting patients with acute left ventricular failure, dobutamine's effects may be deleterious in exercising patients with chronic ischemic heart disease.
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PMID:The effect of dobutamine on exercise performance in patients with symptomatic ischemic heart disease. 669 Dec 44

On the basis of clinical examination and the results of bicycle ergometry and echocardiography in 58 patients with chronic ischemic heart disease the authors determined the contingent of patients in whom long-acting nitrates were most effective. The high clinical effectiveness of the agents in patients with symptoms of the initial stage of cardiac insufficiency is proved and the absence of any essential differences between long-acting nitrates in the character of their effect on hemodynamics is shown. It is established that nitroglycerin and long-acting nitrates cause a qualitatively similar effect on myocardial contractile function and intracardiac hemodynamics in patients with ischemic heart disease.
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PMID:[Modern aspects of nitro preparation use]. 678 20

Three children with congenital heart disease died after surgical procedures involving the placement of valved extracardiac conduits; their deaths were caused by myocardial ischemia following coronary artery compression by the metallic stent of the conduit valve. The first and second patients died of acute myocardial ischemia or infarction during the immediate postoperative period, whereas the third patient died of chronic myocardial ischemia and progressive heart failure several months after the operation. In a fourth patient the problem of possible coronary artery compression was suspected on completion of the surgical procedure, and the valve stent was then repositioned away from the coronary artery; this resulted in marked hemodynamic improvement. Fatal myocardial ischemia from coronary artery compression is a rare but potential complication of valved extracardiac conduit placement in children with congenital heart disease. Preoperative assessment of coronary artery distribution is indicated in those patients with prior intrapericardial operations and subsequent pericardial adhesions. Such assessment in previously unoperated patients may be undertaken at the time of conduit operation. Proper conduit placement and intraoperative recognition of possible coronary artery compression by the conduit are important in preventing significant ischemic complications.
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PMID:Coronary artery compression with fatal myocardial ischemia. A rare complication of valved extracardiac conduits in children with congenital heart disease. 683 74

The workup of a patient with chronic ischemic heart disease (IHD) before the selection of medical-surgical or medical therapy depends on multiple objective and subjective factors. These include symptoms, extent of anatomic disease (degree of coronary arteriosclerosis and left ventricular abnormalities), objective evidence of ischemia, extent of left ventricular dysfunction, and recent intercurrent ischemic events. In a minority of patients, a single factor is of overwhelming importance; e.g., the presence of severe left main coronary artery narrowing in a symptomatic patient indicates surgery is a better choice, whereas evidence of advanced left ventricular dysfunction suggests that surgery is likely to be risky and of limited help to the patient. In most instances, multiple factors should be considered before making a recommendation. The patient should be placed in the appropriate clinical subset and the objective factors that are most important in determining survival should be evaluated. Hence, an exercise electrocardiographic study to evaluate symptoms and exercise tolerance in a patient with angina pectoris and radioventriculographic studies with exercise to estimate left ventricular performance in a patient who complains of fatigue and breathlessness are superior to the subjective interpretations of routine clinical examinations. Asymptomatic patients and those with excellent exercise tolerance pose the most difficult decisions. Perhaps serial (even annual) noninvasive evaluation is appropriate in such patients in light of the current uncertainty about how to manage them. Laboratory tests should be used selectively, systematically and sequentially. The high cost of many of the examinations is reason to avoid duplication. When noninvasive evaluation can answer the question being posed and the cost of hospitalization avoided, this should be done. However, there is little reason to perform noninvasive examinations that do not answer the clinical question being asked; hence, in many patients it is appropriate to proceed directly to coronary arteriography rather than to perform a variety of "screening" examinations before this procedure.
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PMID:The reasonable workup before recommending medical or surgical therapy: an overall strategy. 697 29

A complete discussion of factors involved in causing acute myocardial infarcts is contained in ths review, and a detailed discussion of various complications of acute myocardial infarction is also provided. Interventions that are capable of reducing infarct size in animal models with experimentally produced acute myocardial infarcts are discussed, and factors that might alter infarct size in patients are reviewed. Prognostic factors that allow one to identify high risk patients with acute myocardial infarction following their hospital admission and in the follow-up period after hospital discharge are identified. The need to develop more accurate measurements of the extent of myocardial infarction and myocardial ischemia, and to develop additional prognostic markers that allow one to separate patients most at risk for sudden death and new myocardial infarction from those with ongoing chronic ischemic heart disease and those without additional complications from their ischemic heart disease is also emphasized in this review.
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PMID:Cause and course of acute myocardial infarction. 700 82

The serum lipoprotein profile was determined in 37 patients with chronic ischemic heart disease (IHD) and 100 practically healthy subjects, aged from 18 to 45. HLP was found in 59.5 per cent of the patients examined, 50 per cent in males and 100 per cent in females. Type IV has the highest incidence (54.5%), followed by type IIB(36.4%) and type IIa (9.1 per cent). In 27 per cent of the patients with no HLP determined, less significant changes in LDLP and VLDLP were found, admitted to be dyslipoproteinemia (DLP). HLP and DLP were confirmed in 86.5 per cent of the patients examined. In all patients serum concentration of HDLP-Chol was decreased (mostly in DLP and type IV HLP), whereas the level of HDLP-Tg was increased in most of the cases. As a result, the intralipoprotein index 1(2)(=HDLP-Chol/HDLP-Tg) was decreased, reaching the lowest values in IIa and type IV HLP. The only index of all studied, being changed (elevated) with a statistical significance in all groups of patients with IHD, in those with normolipoproteinemia (NLP) including, was the lipoprotein index II(=LDLP-Chol and VLDLP-Chol/HDLP-Chol). With the morbid process progressing, assessed by ECG data, the functional stage of stenocardia, the degree of the constriction and the number of the pathologically altered coronary arteries, the incidence of NLP, DLP and type IV HLP distinctly decreased, whereas IIa and IIB type HLP increased.
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PMID:[Changes in serum lipoproteins in patients with ischemic heart disease at an early age]. 710 95


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