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)

To clarify the types and frequency of myocardial fibrosis and vascular lesions caused by different types of the rheumatic valvular disease, 41 autopsied hearts with rheumatic valvular lesions were examined and the following results were obtained. As to myocardial fibrosis, 1) perivascular fibrosis, caused mainly by perivascular inflammation and partly by myocardial strain, varied in grade according to the types of the valvular disease, i.e., most severe in mitral regurgitation (MR) and combined valvular disease (CVD) and least in mitral stenosis (MS); 2) Aschoff's nodes: 3 typical and 8 atypical cases were found; 3) perimycial fibrosis due to myocardial strain: most severe in MR and CVD and least in MS; and 4) irregular patchy fibrosis, caused mainly by myocarditis and partly by ischemia, was noticed in all types of the valvular disease. As to vascular lesion, 1) angitis was found in 7 cases and most frequently in MR; and 2) thickening of the intima and media was found in all types of valvular disease. Thus, myocardial fibrosis and vascular lesion varied according to the types of valvular disease, and not only hemodynamic changes but also myocardial fibrosis and vascular lesions might determine the prognosis of the valvular disease.
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PMID:Histopathological studies on the myocardial fibrosis and vascular lesion of rheumatic valvular disease. 732 Nov 53

Idiopathic dilated cardiomyopathy (IDC) accounts for 25% of cases of heart failure in the United States. Understanding the relationship between an inciting event or agent and the development of IDC has progressed only recently. Once IDC has developed, treatment is palliative and little can be done to alter the natural course of the disease. Active myocarditis, a suspected precursor of IDC, is myocardial inflammation and injury without ischemia. The disease ranges from a self-limited flulike illness to one of serious consequence with arrhythmias, heart failure, or death. Many agents have been associated with myocarditis, and the clinical manifestations depend on an interplay between the inciting agent and the host response. The development of a murine model and the expanded use of endomyocardial biopsy using the Dallas criteria have increased our understanding of myocarditis and its sequelae. Therapy consists of managing symptoms using conventional medical regimens for heart failure. Immunosuppressive therapy should be reserved for patients with biopsy-proven disease who have failed conventional therapy. Continued deterioration warrants ventricular assistance and consideration of cardiac transplantation.
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PMID:Myocarditis and idiopathic dilated cardiomyopathy. 765 92

A 31-year-old woman with systemic lupus erythematosus (SLE), diabetes mellitus, and chronic renal failure developed digital ischemia, myocardial dysfunction, abnormal ECG, and elevated CPK levels. Radiographic studies revealed calcification of the peripheral vasculature although coronary angiography was unremarkable. An endomyocardial biopsy demonstrated intra and extracellular myocardial calcification without evidence of vasculitis or primary myocarditis. A diagnosis of calciphylaxis, as a result of secondary hyperparathyroidism, was made. This case demonstrates that calciphylaxis can mimic the cardiovascular manifestations of SLE. Early differentiation of these disparate diseases is important because treatment strategies employed in SLE may exacerbate calciphylaxis.
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PMID:Systemic lupus erythematosus: calciphylaxis induced cardiomyopathy. 769 81

Cardiac complications of cocaine abuse and a rational approach to evaluating and managing them are described. Cardiac abnormalities reported among asymptomatic cocaine abusers include echocardiographic left ventricular hypertrophy and segmental wall motion abnormalities. Electrocardiogram may reveal increased QRS voltage, ST-T changes, and pathologic Q waves. Episodes of ST elevation may be seen during Holter monitoring. The management of cocaine-abusing patients who present to an emergency room with acute chest pain is controversial because the two reported studies yielded conflicting results regarding the incidence of myocardial infarction (MI). Even in the absence of infarction, electrocardiographic abnormalities are common among these patients, which complicates the decision-making regarding hospitalization. Pathophysiology of cocaine-related MI is discussed. Distinct clinical features of cocaine-related MI make it clear that the association between the two is not just temporal. However, considering the number of persons abusing cocaine, it is a rarity. Beta-adrenergic blockers should be avoided in the treatment of cocaine-induced myocardial ischemia which is best treated with nitrates and calcium-channel blockers. Reports of cocaine-induced myocarditis and cardiomyopathy are reviewed. Experimental studies and clinical case reports suggest that cocaine may cause lethal arrhythmias. Cocaine prolongs repolarization by a depressant effect on potassium current and may generate early afterdepolarizations. It is possible that cocaine-associated arrhythmias are secondary to vasospasm-related ischemia and reperfusion as well.
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PMID:Cardiac complications of cocaine abuse. 772 Feb 92

Cocaine use is accompanied by a high risk of serious adverse effects involving the cardiovascular system. The basic cellular mechanisms of cocaine consist in [1] a potentiation of catecholamine effects by inhibition of the presynaptic uptake carrier [2] local anesthetic effects by the block of sodium-channels. Acute ischemic events can be induced by cocaine through coronary spasms in a situation of physiologic stress already accompanied by an enhanced myocardial oxygen demand. Procoagulant properties of cocaine may, moreover, favor coronary thrombosis formation and the development of myocardial infarction. Ischemia, reperfusion and the direct action of catecholamines on cardiocytes are accompanied by enhanced cytoplasmic calcium levels, inducing delayed after-potentials, repetitive action-potential generation and premature ventricular beats. Conduction velocity impairments caused by the local anesthetic effects of cocaine and inhomogeneous repolarization phenomena related to potassium channel inhibition may form a substrate for re-entrant circuits inducing ventricular fibrillation. Cocaine abuse may also cause degenerative and inflammatory alterations of the myocardium. Besides secondary ischemic changes, hypersensitivity-myocarditis and toxic cardiomyopathies that may be due to the cardiotoxic effects of catecholamines have been described in cocaine abusers. Moreover, persons using cocaine intravenously seem to be particularly endangered by bacterial endocarditis compared to the users of other intravenous drugs, for still unknown reasons.
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PMID:The pathophysiology of cocaine cardiotoxicity. 786 5

Myocardial fibrosis in patients with hypertrophic cardiomyopathy (HCM) may play an important role in the function and/or dimensions of the left ventricle. We present an autopsied case of HCM followed for 10 years. A 68-year-woman with HCM underwent trans-aortic myectomy of the interventricular septum in 1979. A significant amount of round cell infiltration, myocardial fibrosis and disarray were observed in the resected specimen. She experienced repeated admissions due to diabetes mellitus and congestive heart failure, and died of renal failure in 1989. An autopsy revealed extensive myocardial fibrosis and significant cell infiltration in the ventricular myocardium. The infiltrating cells were almost all lymphocytes, and the ratio of CD4 to CD8 was 3.8. This ratio was different from that of typical viral myocarditis. This case suggests that there may be an undefined inflammatory process causing fibrosis in HCM, in addition to the ischemia due to intramural small coronary artery stenosis.
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PMID:An autopsy case of hypertrophic cardiomyopathy with pathological findings suggesting chronic myocarditis. 820 86

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

A certain group of compounds often derived from microbes known as ionophores function as ion channels when incorporated in biological membranes. Different ionophores have a relative specificity for certain cations such as Ca2+ or K+. When such compounds are integrated in the cell membrane of a host cell a leakage of the ion in question is induced and the physiologic ion gradient will be dissipated. This will activate ion pumps at the expense of ATP in order to restore the physiologic ion gradient. This effect is seen for a number of different viruses including Coxsackie B3. Based on own experiments we suggest that this ionophoric effect is important in the pathophysiology of myocarditis. We have shown that mice with Coxsackie B3 myocarditis have low myocardial ATP and high ADP and AMP levels. This pattern of abnormal energy metabolism is also seen in patients with Syndrome X. It is suggested that the ECG and thallium perfusion scintigram suggestive of ischemia in such patients is rather due to the effect of an ionophore leading to an extracellular potassium shift.
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PMID:Ionophoric interaction with the myocyte sarcolemma: a new insight into the pathophysiology of degenerative myocardial disease. 839 Jul 16

Congestive heart failure represents the most common medical hospital discharge diagnosis, and can occur in patients with preserved indexes of left ventricular systolic function, even in absence of patent coronary or valvular heart disease. The present review examines the role of imaging techniques in the diagnosis and follow-up of these patients. Imaging of the heart has undergone dramatic advances with the development and refinement of new imaging modalities such as echocardiography, computed tomography, magnetic resonance and radionuclide emission tomography. The role of "low-tech" modalities such as chest roentgenogram is discussed. The possibilities offered by ultrasounds or magnetic resonance in tissue characterization are then compared with the actual capability of cardiac imaging in detecting myocardial tissue alterations (oedema, ischemia, myocarditis, etc.) and/or degeneration (fatty degeneration, fibrosis, amyloidosis, etc.). Finally, the potential use in modern clinical medicine of magnetic resonance spectroscopy and positron emission tomography to study myocardial metabolism and cellular function are discussed.
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PMID:[The remodelling of the heart in heart failure: from thoracic radiography to magnetic resonance]. 849 59

Cardiac toxicity and hemodynamic alterations are frequently associated with high-dose interleukin-2 (IL-2) immunotherapy in cancer patients. Serious cardiac events including myocardial infarction, ischemia, and noninfectious myocarditis have been observed. We document two cases of unusually severe but reversible cardiac abnormalities related to IL-2 therapy: one patient with a profound form of global myocardial hypocontractility and a second patient with regional aneurysmal and dyskinetic changes of the left ventricle. These cases exhibit unique features not previously described in IL-2-treated patients. The possible pathophysiologic mechanisms underlying these global and regional forms of cardiomyopathy, including the production of secondary-messenger molecules such as nitric oxide and myocardial stunning, are discussed. Both patients remain disease free of their cancer (> 3 years since completing therapy), are without residual cardiac dysfunction or recurrent related symptoms, and have not experienced any additional cardiac events. The report demonstrates the complexity of the cardiac toxicities associated with IL-2-based immunotherapy and recognizes a need for treating physicians to be familiar with their management.
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PMID:Severe reversible global and regional ventricular dysfunction associated with high-dose interleukin-2 immunotherapy. 857 67


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