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

Chest pain can arise from cardiovascular or noncardiovascular causes. Among the latter are the skin, the chest wall, intrathoracic structures, or subdiaphragmatic organs. The problem to attribute the chest discomfort to either the heart or extracardiac organs arises because the heart, pleura, aorta, and esophagus are all supplied by sensory fibers from the same spinal segments. In contrast to the diseases mentioned above, angina pectoris in sensu strictu is defined as chest pain or discomfort of cardiac origin that arises because of temporary imbalance between myocardial oxygen supply and demand. The metabolic oxygen requirements of the myocardium are essentially dictated by myocardial contraction since only a fraction of the consumed oxygen is needed by the quiescent heart. Therefore, the factors that primarily influence myocardial oxygen consumption include heart rate, the force of cardiac contraction, and myocardial wall tension, as determined by pressure (afterload), volume (preload), and wall thickness. Extracoronary diseases, e.g. hypertensive heart disease, aortic stenosis or cardiomyopathies, can influence these factors and induce angina pectoris (Figure 1). On the other hand, different diseases influencing the oxygen supply, e.g. anemia, can cause angina pectoris, too. In addition, the modulation of the coronary tone by mediators and cytokines can cause angina, coronary spasm being one example. The neurophysiological substrate of angina pectoris are ganglia which are present within the heart, particularly in epicardial fat. The sympathetic nervous system is the main conveyer of afferent pain fibers from the heart and pericardium, but many fibers may travel by the vagus and the phrenic nerves. Therefore, multiple thoracic structures may cause similar pain syndromes in the distressed patient. The blood supply of intrinsic cardiac ganglia arises primarily from branches of the proximal coronary arteries. Adenosine, among a number of substances, can modulate the activity generated by cardiac afferent nerve endings and intrinsic cardiac neurones. During myocardial ischemia adenosine is released in large quantities into the interstitial space. Given as an intravenous bolus to healthy volunteers or to patients with ischemic heart disease and angina pectoris, adenosine provokes angina pectoris-like pain, which is similar to habitual angina pectoris with regard to quality and location. But other mediators (e.g. bradykinin, histamine, prostaglandins, potassium, lactate) can be involved in the development of angina pectoris, too. As most emphasis should be given to the most serious causes first, the cardiologist has to consider ischemic cardiac disease in the differential diagnosis of nearly every case of acute chest pain. The differential diagnosis contains several causes of nonischemic cardiac chest pain. Dissecting aortic aneurysm may cause severe anterior chest pain that can be mistaken for myocardial infarction. Patients frequently will note the sudden onset of the pain rather than the relatively slower onset of ischemic pain. Furthermore, they feel as a tear and describe it as the most severe pain they have ever had. Pericarditis can be characterized as a sharp precordial knife-like pain that is often increased by lying down, breathing, swallowing, or any other thoracic motion. Radiation of pericardial pain is often relieved by sitting up or leaning forward. It may involve the shoulders, upper back, and neck because of the irritation of the diaphragmatic pleura. Acute pulmonary embolism is associated with severe chest pain. It may mimic acute myocardial infarction. Pulmonary embolism should be suspected when dyspnea or tachypnea seems to be disproportionate to the severity of the chest pain. Diffuse esophageal spasm is the extracardiac condition that is confused most often with ischemic cardiac chest pain. This pain presents as a deep thoracic pain that may be present over most of the thorax. It may extend down the anterome
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PMID:[Angina pectoris in extracoronary diseases]. 1037 99

Twenty years ago, I became an "unstable patient", starting with a short episode of precordial discomfort and tiredness, ischemic ECG without enzymes, hypokinetic apex and no other signs. Following a week in bed and a lot of sleep, I went back to my usual lifestyle, refusing to undergo cineangiography or any hydraulic intervention. For ten years, the periodic controls showed no changes and I continued my intense activity under adequate therapy until another more severe episode occurred. Again, during a stressful and psychologically negative period, I experienced more severe precordial discomfort that was accentuated after minor psychological tension, whereas long and intense physical exercise was instead asymptomatic. The hypokinetic area was more extensive--no enzymes again--with a more severe ischemic ECG. My inability to face my psychological stress suggested surgical bypass, given the fact that since the Fifties, any type of intervention--even if nothing is vascularized--would nevertheless block pain and allow me to return to a normal lifestyle (denervation). At that time, cineangiography showed the occlusion of all three main coronary arteries. These occlusions had been there for years without an infarct and were obviously already compensated by adequate collateral circulation, as demonstrated by the normal lifestyle I had led with intense and long-lasting physical exercise. I returned to my regular activity, again mainly under anti-adrenergic stress therapy, and now, another ten years after surgery, I am still waiting for a third episode or something else. What have I learned from studying myself? I've learned that every ischemic patient has his own history and must learn how to face his own risks, the different patterns of so-called ischemic heart disease can not be theorized in a unique etiopathogenesis, the adrenergic system plays a major role in this disease, the "plumbing" vision is supported by reasons which have little to do with the knowledge--as yet incomplete--of the natural history of this disease, and the data obtained in years of research have been confirmed.
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PMID:[What I have learned by monitoring my own ischemia]. 1054 37

It is well known that thyrotoxicosis may elicit acute myocardial ischemia even in patients with angiographically normal coronary vessels. The involved mechanisms are not clearly defined although some hypothesis have been suggested. We report a case of a 54-year-old woman affected by Graves' disease with thyrotoxicosis which was referred to our Institute because of unstable angina. During hospitalization a two dimensional echocardiogram, performed during chest discomfort, showed left ventricular apical akinesis and impaired global systolic function. A subsequent coronary angiography revealed normal epicardial vessels. She was successfully treated with high-dose methimazole and propranolol and a repeat echocardiogram evaluation showed normalization of left ventricular systolic function. Six months later, because of the appearance of paroxysmal atrial fibrillation, the patient underwent total thyroidectomy and a substitutive therapy with L-T4 (100 micrograms/die) was started. The authors review the possible mechanisms involved in the pathogenesis of myocardial ischemia during thyrotoxicosis.
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PMID:Thyrotoxicosis, unstable angina and normal coronary angiogram. 1060 35

Iodine-131 (I-131) ablation of thyroid remnant and/or persistent, recurrent or metastatic tumour is part of the initial and subsequent management of well-differentiated thyroid carcinoma. Key to optimizing the safety and efficacy of radioablation is maximizing the selective uptake of radioiodine by normal or neoplastic thyroid tissue. This is achieved by ensuring adequate serum concentrations of thyroid-stimulating hormone (TSH). Exogenous TSH administration obviates the thyroid hormone suppression therapy withdrawal that is necessary for endogenous TSH elevation. It also avoids the marked morbidity, discomfort, and impairment in professional and educational pursuits and quality of life that often result from such withdrawal. Multicentre clinical studies have documented the safety and efficacy of recombinant human TSH (rhTSH) in promoting radioiodine uptake in the diagnostic scanning of well-differentiated thyroid cancer. Study of the use of rhTSH to facilitate radioablation of remnant and malignant thyroid tissue is at an earlier stage, with formal clinical investigation underway. Since April 1995, however, rhTSH has been employed as a radioablative adjunct in over 100 patients in the manufacturer's Compassionate Use Program. Twelve of these cases, reported or reviewed in the present paper, provide preliminary evidence that rhTSH is safe and effective in the radioablation setting. More data are needed to confirm these observations and to provide guidelines for optimal radioiodine dosing, and should be furnished by ongoing clinical investigation. rhTSH is the only acceptable treatment option in a subgroup of patients with well-differentiated thyroid cancer, including those with hypopituitarism, ischaemic heart disease, a history of "myxoedema madness," debilitation due to very advanced disease or inability to produce TSH due to continued production of thyroxine by thyroid remnant or metastatic tumour. Therapeutic use of rhTSH may be considered in an increasing number of other cases.
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PMID:Recombinant human thyroid-stimulating hormone (rhTSH) in the radioablation of well-differentiated thyroid cancer: preliminary therapeutic experience. 1072 3

Two women with myotonic dystrophy underwent dipyridamole thallium-201 (201Tl) myocardial perfusion imaging, after which one patient developed flat T waves in lead I and aV(L), and inverted T waves in leads V(2-6). The other patient developed a nonspecific intraventricular block that progressed to complete left bundle branch block and was associated with chest discomfort. Reversible scintigraphic defects were observed in both women. Although there was evidence that suggested myocardial ischemia on the ECG changes and 201Tl scintigraphic findings, coronary angiography demonstrated no significant stenoses in either patient. These findings suggest that microvascular dysfunction may lead to myocardial ischemia and conduction disturbances in patients with myotonic dystrophy.
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PMID:Microvascular ischemia in patients with myotonic dystrophy. 1098 60

In every year since 1984, cardiovascular disease has claimed the lives of more females than males. More than 450,000 women succumb to heart disease annually, and 250,000 die of coronary artery disease. Despite the proportions, most women believe they will die of breast cancer. The perception that heart disease is a man's disease and that women are more likely to die of breast cancer is alarming. Although women develop heart disease about 10 years later than men, they are likely to fare worse after a heart attack. The poorer outcomes are due, in part, to the failure to identify heart attack symptoms. Approximately 35% of heart attacks in women are believed to go unnoticed or unreported. However, because of increased age, women are more likely to have co-morbid diseases such as diabetes and hypertension. In women, not only is "tightness" or discomfort in the chest a warning sign, but in addition, nausea and dizziness are common indicators of myocardial ischemia. Other symptoms include breathlessness, perspiration, a sensation of fluttering in the heart, and fullness in the chest. In comparison to men, women are less likely to undergo tertiary care interventions such as cardiac catheterization, angioplasty, thrombolytic therapy, and bypass surgery; to participate in cardiac rehabilitation; and to return to work full-time after myocardial infarction. In the past, most research about treatments for heart disease focused on men, and gender differences have been ignored. Recent studies are enrolling enough women to test if there are differences between men and women in outcomes. One of the major areas of research relates to estrogen and hormonal replacement therapy to reduce the relative risk of heart attack and stroke. The Women's Health Initiative is a major NIH-sponsored trial that addresses the issue of primary prevention of cardiac disease by hormonal replacement therapy. The results will be available in 2004. The Heart Estrogen/Progestin Replacement Study (HERS), disappointingly, did not show a significant reduction of coronary events in women taking hormonal replacement therapy, nor did the Estrogen Replacement and Atherosclerosis (ERA) trial of 309 postmenopausal women who underwent coronary angiography. New insight into the role of vitamins, phytoestrogens and other natural sources, and selective estrogen receptor modulators may provide other options for management. Until then, modification of risk factors and healthy life style choices are recommended for reducing the risk of cardiac disease. In fact, the key to a healthy heart in the year 2000 appears closely tied to life style choices. Prevention of disease is the key, and current recommendations are simply to stop smoking, or do not start; treat and control blood pressure >140/90 mm Hg; manage elevated lipids by diet, exercise, and cholesterol-lowering medications (if necessary); treat diabetes; lose weight so that BMI is <25; walk for 20-30 minutes at least three times a week; and take an aspirin tablet daily.
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PMID:Heart disease in women. 1114 May 44

In arid zone of Uzbekistan summer heat discomfort aggravates the course of ischemic heart disease, provokes meteopathic reactions which we call "meteorological strain syndrome". In this season anginal attacks, episodes of arrhythmia and coronary failure become more frequent especially in patients over 70 years of age and migrants.
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PMID:[Meteopathogenic mechanisms of exacerbating ischemic heart disease in an arid zone]. 1124 39

CHD is the major cause of morbidity and mortality in the elderly in the U.S. In this age group, the clinical presentation of CHD can be quite atypical. In general, the incidence of typical precordial chest pressure/pain denoting myocardial ischemia is less common whereas dyspnea as an anginal equivalent symptom is frequent. The diagnosis of ischemic cardiac pain is frequently confused by the many comorbid conditions present in the elderly. Even when classic ischemic precordial discomfort is present it tends to be less severe and less well defined. The elderly appear to have reduced pain perception and as a result silent myocardial ischemia is more common and carries a somewhat worse prognosis in the elderly than in younger age groups. Similarly, the presenting symptoms of acute myocardial infarction in the elderly can be nonspecific. The classic crushing substernal chest pain decreases with age whereas the symptom of dyspnea gradually increases. Neurologic symptoms, weakness, and worsening heart failure are common clinical presentations of an acute infarction in elderly patients. Silent (unrecognized) myocardial infarctions are common in the elderly and carry serious prognostic implications.
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PMID:Clinical Presentation of Coronary Artery Disease in the Elderly: How Does it Differ From the Younger Population? 1141 43

Coronary artery disease is the major cause of morbidity and mortality in the elderly in the United States. In this age group, the clinical presentation of coronary heart disease can be quite atypical. In general, the incidence of typical precordial chest pressure/pain denoting myocardial ischemia is less common, whereas dyspnea as an anginal-equivalent symptom is frequent. The diagnosis of ischemic cardiac pain is frequently confused by the many comorbid conditions present in the elderly. Even when classic ischemic precordial discomfort is present, it tends to be less severe and less well defined. The elderly appear to have reduced pain perception; as a result, silent myocardial ischemia is more common and carries a somewhat worse prognosis in the elderly than in younger age groups. Similarly, the presenting symptoms of acute myocardial infarction in the elderly can be nonspecific. The classic crushing substernal chest pain decreases with age, whereas the symptom of dyspnea gradually increases. Neurologic symptoms, confusional states, weakness, and worsening heart failure are common clinical presentations of an acute infarction in elderly patients. Silent (unrecognized) myocardial infarctions are common in the elderly and carry serious prognostic implications.
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PMID:Clinical manifestations of acute myocardial infarction in older patients. 1168 19

A growing number of Japanese patients are being treated with ICDs. Efforts are warranted to minimize the rates of ICD shocks that cause discomfort and anxiety. The circadian distribution of ICD discharges was investigated in 80 patients (57+/-10 years of age, 69 men) from ten Japanese medical centers. The underlying heart disease was ischemic in 27 versus nonischemic in 53 patients. All patients had refractory VT or VF, and received appropriate shocks confirmed by stored data retrieved from the memory of the ICD. In the analysis of 354 appropriate shocks delivered in the overall population, a morning peak in VT or VF episodes was observed. However, subgroup analyses of the circadian distribution of ICD shocks revealed that the morning peak in VT or VF episodes was confined to patients with ischemic heart disease and was blunted by treatment patients with beta-adrenergic blockers. The absence of a morning peak in appropriate ICD shocks among patients with nonischemic heart disease remains unexplained and was unrelated to the use of beta-adrenergic blockers. In conclusion, the circadian pattern of appropriate ICD discharges was related to the underlying heart disease. In patients with ischemic heart disease, recurrences of VT or VF peaked in the morning. In contrast, in patients without ischemic heart disease, the episodes of VT or VF were evenly distributed during waking hours. Beta-adrenergic blockers appeared to blunt the morning peak in VT or VF among patients with ischemic heart disease.
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PMID:Absence of a morning peak in ventricular tachycardia and fibrillation events in nonischemic heart disease: analysis of therapies by implantable cardioverter defibrillators. 1181 28


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