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)

Exercise echocardiography, a versatile, noninvasive diagnostic test of left ventricular wall motion performed at rest and under induced stress, enables the cardiologist to detect and assess coronary artery disease. Stress-induced ischemia is thereby expressed as left ventricular regional wall motion abnormality. By using various physical (bicycle or treadmill exercise) and pharmacological (dipyridamole, dobutamine, adenosine) stress inducers, the test provides information about the localization and extent of coronary artery disease in addition to detecting stress-induced coronary insufficiency. As regards diagnostic accuracy in detecting coronary artery disease, stress echocardiography is superior to exercise electrocardiography and, according to the available data, it is comparable to perfusion scintigraphic testing. Studies have demonstrated the clinical value of stress echocardiography in detecting residual stenosis after angioplasty, for diagnosing bypass dysfunction after heart surgery, for preoperative risk assessment in noncardiac surgeries, and for obtaining prognostic information, e.g., after myocardial infarction. Preliminary studies have shown that pharmacological exercise echocardiography is able to identify viable myocardium in the early phases after acute myocardial infarction. Furthermore, it is able to predict the functional success of revascularization in chronic regional left ventricular dysfunction. In addition to the wide range of diagnostic possibilities in coronary artery disease, other notable applications include stress testing for assessment of global left ventricular pump function in patients with aortic regurgitation or cardiomyopathy.
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PMID:[Stress echocardiography--an evaluation of current status]. 797 3

Three cases of diabetic myocardiopathy having history of diabetes, angina and left ventricular dysfunction of various degrees and confirmed by coronary angiography and endomyocardial biopsy were reported. Electrocardiography showed significant ST-T changes simulating coronary insufficiency but without definite localization. As to the treatment, nitrate preparations, inotropic agents such as strophanthin K, digoxin etc. were used to relieve the symptoms; insulin was also administered to control the blood glucose level. Diltiazem, a calcium blocker, is also of help in alleviating the symptoms. It is shown in the present study and in the literatures as well that diabetic myocardiopathy is a disease showing intramural microvascular endothelial proliferation and swelling as well as subendothelial accumulation of acid glycogen deposition cells. The transportation of intracellular calcium ions and the cellular metabolism are thus affected, so there are extensive ischemia, focal necrosis and fibrosis in the myocardium with resulting cardiac dysfunction. The authors are, therefore, of the opinion that diabetic myocardiopathy is a specific and separate clinical entity.
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PMID:[Diabetic myocardiopathy]. 804 81

Lipoprotein lipase (LPL) may play an important role in myocardial metabolism by releasing free fatty acids from triglycerides for oxidation by myocytes. However, studies in species other than humans have differed in their conclusions as to whether LPL is produced by cardiac myocytes or interstitial cells. The location and source of LPL in human myocardium were determined on formalin-fixed samples from 25 cardiomyopathy patients and seven control patients. LPL protein was detected immunohistochemically on cardiac myocytes, adipocytes, and endothelial cells, as well as on interstitial cells consisting of both vascular pericytes and smooth muscle cells. In all 32 patients, in situ hybridization localized LPL mRNA to cardiac myocytes and adipocytes, but LPL mRNA was not detected in interstitial cells. Quantitative in situ hybridization failed to reveal correlations between LPL mRNA levels and New York Heart Association functional class, left ventricular ejection fraction, or beta-adrenergic agonist therapy. Also, quantitative in situ hybridization demonstrated apparently linear loss of detectable myocardial mRNA after onset of ischemia, with a disappearance half-time of approximately 26 hours. In summary, LPL is produced primarily by cardiac myocytes rather than by interstitial cells in human myocardium. Furthermore, LPL protein is present on cells with and without detectable LPL mRNA, suggesting that LPL is translocated from sites of synthesis to sites of utilization.
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PMID:Lipoprotein lipase is produced by cardiac myocytes rather than interstitial cells in human myocardium. 806 6

Recent advances have been made in understanding Kawasaki disease, acute rheumatic fever and rheumatic heart disease, cardiomyopathy, and acquired immunodeficiency syndrome. Immune-mediated tissue injury in Kawasaki disease is likely caused by response to a superantigen. Persistent functional and anatomic coronary abnormalities may lead to silent ischemia and increase the risk of early atherosclerotic heart disease. Intravenous immunoglobulin therapy is clearly beneficial, but specific therapy awaits further definition of the etiology and pathophysiology of Kawasaki disease. Recently updated diagnostic criteria for Kawasaki disease and acute rheumatic fever are discussed. Advances in the understanding of genetically determined abnormal immune responses to streptococcal pharyngitis may help explain acute rheumatic fever manifestations. Further advances have been made in the elucidation of the pathophysiology of cardiomyopathy, particularly the role of viruses and genetic factors. Angiotensin-converting enzyme inhibitors appear to improve survival in dilated cardiomyopathy. Controversy regarding the possible myocardial depressant effect of zidovudine in human immunodeficiency virus infection is discussed.
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PMID:Acquired heart disease in children. 819 64

It has been clearly established that ischemic heart disease, hypertension and ageing affect diastolic function before any change is observed in contractile function. Though an increasingly recognised clinical entity, cardiac failure with normal systolic function still does not have any specific treatment. Phosphodiesterase inhibitors which increase AMPc, in addition to their inotropic and vasodilator effects, accelerate relaxation. Major and isolated abnormalities of relaxation have been demonstrated in vitro in non necrosed tissues of both the dilated and hypertrophic forms of advanced cardiomyopathy. The myocardium seems unable to restore rapidly the low cytosolic calcium concentrations required for the deactivation of the contractile proteins. The underlying mechanisms are probably very complex but a deficit in AMPc production has been demonstrated in very advanced stages of cardiomyopathy. In ischemia, however, the abnormalities of relaxation seem to be directly related to a defect in free energy production inhibiting the sarcoplasmic reticulum calcium pump. If abnormalities of relaxation due to ischemia and those due essentially to a passive mechanism are excluded, phosphodiesterase inhibitors would seem to have pharmacological effects likely to improve diastolic function. Clinical studies confirm the beneficial effects of Milrinone and Enoximone on relaxation and the rapid phase of diastolic filling, both in acute and chronic studies. However, it has not yet been clearly established whether improved diastolic function is due to a direct action on the myocardium or an indirect action due to improved conditions of load. In order to determine the specific effects of phosphodiesterase inhibitors on diastolic function, further research is required.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Effects of phosphodiesterase inhibitors on diastolic function]. 821 93

The role of symptoms in establishing a diagnosis in cardiovascular diseases has decreased. Treatment privileges action and underestimates the potentially favourable spontaneous outcome of the treated condition. The object of this article is not to question the progress made in presymptomatic diagnosis of certain cardiovascular diseases or the benefits of treatment prescribed for some a- or paucisymptomatic patients: recent reports, particularly in asymptomatic aortic regurgitation, silent ischemia and subclinical left ventricular dysfunction of cardiomyopathy have confirmed the utility of therapy in these cases. However, the risks of misinterpreting a symptom and the natural history should be underlined: the "complaint" of the patient not properly assessed; cascades of "complementary investigations" of debatable utility and uncertain interpretation, when taken out of context; substitution of the medical therapeutic offer on demand of the patient and inadequate patient education concerning possible therapeutic approaches: the quest for intermediary objectives (anatomic, physiologic, biologic), which have not been shown to increase the quality or duration of life; the disproportion between the small number of validated therapies and the ever increasing range of interventional audacities in asymptomatic patients... It is important that general pathology and the natural history of cardiovascular diseases are taught again in France. With respect to symptoms, proper assessment no longer depends on "clinical judgment"; it should have a greater role in diagnosis of cardiovascular diseases by the understanding of the physiopathological mechanisms, Bayesian assessment of its predictive value, and accurate inclusion in multiparameter scores derived from recent large scale epidemiologic and therapeutic trials.
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PMID:[Symptoms and natural history of cardiovascular diseases: obsolete?]. 827 55

After decades of focus on the effects of cocaine abuse on the central nervous system (CNS), the cardiovascular toxicity of cocaine is just beginning to be appreciated. The most common cardiovascular pathologies associated with cocaine use include: cardiomyopathy, left ventricular dysfunction, myocarditis, arrhythmia, hypertension, myocardial infarction, stroke, arterial thrombosis, deep vein thrombosis, and gastrointestinal, renal, and skeletal muscle ischemia. This article reviews the above pathologies with speculations on the mechanisms by which cocaine produces cardiovascular tissue damage.
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PMID:Cardiovascular and thrombosis pathology associated with cocaine use. 829 12

In-hospital and late complications related to percutaneous placement of 240 intraaortic balloon pump catheters in 231 consecutive patients from March 1985 through June 1990 were reviewed. Mean age was 64 +/- 11 years and 34% were women. Average duration of counterpulsation was 44.2 hours. Indications for counterpulsation included complications of myocardial infarction (34.6%), prophylactic placement before high-risk coronary angioplasty (20.0%) or open heart surgery (12.9%), complicated coronary angioplasty (18.3%), end-stage cardiomyopathy (5.4%) and miscellaneous (8.8%). Early major complications occurred in 11 cases (4.6%) and included limb ischemia requiring surgery (n = 9), bleeding requiring arterial repair (n = 1) and septicemia (n = 1). Other complications included hematoma requiring transfusion (n = 7), limb ischemia resolving with balloon catheter removal (n = 12), and superficial wound infection (n = 1). Overall in-hospital complication rate was 13% (31 of 240). Peripheral vascular disease and diabetes were found to be significant predictors of limb ischemia (p = 0.01 and p = 0.02, respectively). Follow-up information was obtained in 97% of patients with a mean duration of 19 months: 2 patients (1.1%) required vascular surgery for femoral false aneurysms and 1 patient experienced new onset of claudication. In conclusion, compared with previous experience, contemporary intraaortic balloon counterpulsation with percutaneous placement of smaller size (8.5Fr to 10.5Fr) catheters is associated with improved complication profile. This will further enhance the current trend for an expanding role of intraaortic balloon counterpulsation in complex interventional procedures.
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PMID:Complications associated with percutaneous placement and use of intraaortic balloon counterpulsation. 842 77

A male patient presented with symptoms of angor under effort. Echocardiography and angiocardiography revealed apical hypertrophic myocardiopathy, associated with multiple fistulas connecting the anterior descending coronary artery and right coronary artery with the cavity of the left ventricle, as demonstrated by coronariography. We comment on the hypothesis that support a causal relationship between the two anomalies, microfistulas being the possible cause of the reactive hypertrophy through the induction of a coronary steal phenomenon with local ischemia; alternatively, the myocardiopathy itself might be the cause of microfistulas formation by inducing an anomaly in the Thebesius venous system. A pathogenic relationship is suggested between the syndrome of angor and these two rare pathological entities.
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PMID:[Apical hypertrophic myocardiopathy and multiple fistulae between the coronary vessels and the left ventricle]. 853 48

Collagen which is present in the myocardium in relatively small amounts is the most abundant structural protein of the connective tissue network. Its structural organization consists of a complex weave of collagen fibers that surrounds and interconnects myocytes, groups of myocytes, muscle fibers and muscle bundles. The conformation of interstitial fibrillar collagen makes it highly resistant to degradation by all proteinases other than specific collagenases. In hearts with myocardial damage secondary to myocardial infarction, chronic ischemia, inflammation, or cardiomyopathy, a complex sequence of compensatory events occur that eventually result in an adverse left ventricular remodeling. This continual state of remodeling is characterized by persistent collagenase activity, fibrillar collagen degradation, and progressive myocyte loss. The net effect is a shift in the balance between collagen synthesis and degradation which leads to an inadequate fibrillar collagen matrix, progressive ventricular dilatation and sphericalization with wall thinning and eventual congestive heart failure.
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PMID:Ventricular remodeling in heart failure: the role of myocardial collagen. 854 Apr 1


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