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Query: UMLS:C0018799 (heart disease)
 34,133 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

An important issue for the understanding of the host-parasite relationship in Chagas' disease is the extent of the action of the immune system on the parasite. To advance our understanding of this aspect, we evaluated the effect of leukocytes and/or sera from patients with Chagas' disease on trypomastigotes of Trypanosoma cruzi. We incubated, in vitro, leukocytes and sera, from patients with Chagas' disease without evidence of heart disease (INF), patients with Chagasic cardiopathy (CDM) and healthy controls (VOL), with trypomastigotes at 37 degrees C for three hours. Mice were inoculated with parasites at the end of the incubation. We kept a record of the survival time of each animal and every three days we evaluated their Parasitemia. INF (36.4%) and CDM (42.9%) prolonged the prepatent period, but not Vol. Only CDM (57.1%) extended the survival time. The sera from CDM patients that extended the survival of mice prolonged the prepatent period. However serum alone did not extend the survival time, providing evidence that leukocytes are required to decrease the virulence of the inoculum. The capacity of leukocytes and sera, from CDM, to prolong survival time shows that the immune system of patients with Chagasic cardiomyopathy can affect the parasite more intensely than IFN. On the other hand, the higher frequency of positive xenodiagnosis in CDM (11), suggests that, in vivo, occur a down regulation of the immune response.
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PMID:Trypanosoma cruzi: infectivity and virulence of trypomastigotes incubated with leukocytes and serum from patients with Chagas' disease. 134 41

It is clear that cocaine has cardiotoxic effects. Acute doses of cocaine suppress myocardial contractility, reduce coronary caliber and coronary blood flow, induce electrical abnormalities in the heart, and in conscious preparations increase heart rate and blood pressure. These effects will decrease myocardial oxygen supply and may increase demand (if heart rate and blood pressure rise). Thus, myocardial ischemia and/or infarction may occur, the latter leading to large areas of confluent necrosis. Increased platelet aggregability may contribute to ischemia and/or infarction. Young patients who present with acute myocardial infarction, especially without other risk factors, should be questioned regarding use of cocaine. As recently pointed out by Cregler, cocaine is a new and sometimes unrecognized risk factor for heart disease. Acute depression of LV function by cocaine may lead to the presence of a transient cardiomyopathic presentation. Chronic cocaine use can lead to the above problems as well as to acceleration of atherosclerosis. Direct toxic effects on the myocardium have been suggested, including scattered foci of myocyte necrosis (and in some but not all studies, contraction band necrosis), myocarditis, and foci of myocyte fibrosis. These abnormalities may lead to cases of cardiomyopathy. Left ventricular hypertrophy associated with chronic cocaine recently has been described. Arrhythmias and sudden death may be observed in acute or chronic use of cocaine. Miscellaneous cardiovascular abnormalities include ruptured aorta and endocarditis. Most of the cardiac toxicity with cocaine can be traced to two basic mechanisms: one is its ability to block sodium channels, leading to a local anesthetic or membrane-stabilizing effect; the second is its ability to block reuptake of catecholamines in the presynaptic neurons in the central and peripheral nervous system, resulting in increased sympathetic output and increased catecholamines. Other potential mechanisms of cocaine cardiotoxicity include a possible direct calcium effect leading to contraction of vessels and contraction bands in myocytes, hypersensitivity, and increased platelet aggregation (which may be related to increased catecholamine). The correct therapy for cocaine cardiotoxicity is not known. Calcium blockers, alpha-blockers, nitrates, and thrombolytic therapy show some promise for acute toxicity. Beta-Blockade is controversial and may worsen coronary blood flow. In patients who develop cardiomyopathy, the usual therapy for this entity is appropriate.
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PMID:The effects of acute and chronic cocaine use on the heart. 134 9

Our purpose in this article is to examine the hypothesis that both myocardial disease and ischemia can alter the electrophysiologic function of the ion channels responsible for the cellular electrical activity of the heart. Changes in the intracellular and extracellular milieus occur during ischemia and can alter the electrophysiology of several species of ionic channels and the cellular electrophysiologic activity of cardiac myocytes. Included are 1) changes in extracellular [K+] and pH and in intracellular [Na+], [Ca2+], and pH; 2) accumulation of noxious metabolic products such as lysophosphatidylcholine; and 3) depletion of intracellular ATP. Finally, ischemia or disease (e.g., hypertrophy) can alter the electrophysiology of at least two types of K+ channels, the A-like channels underlying the transient outward current and the inward rectifier, by mechanisms that apparently do not involve alteration of either the intra- or extracellular milieus. Findings suggest that the expression of cardiac A-like channel function can be altered by hypertrophy and that at least one intrinsic conductance property of the inward rectifier can be altered by ischemia. We speculate that the control of expression, function, and regulation of cardiac ion channels can be affected at the molecular level by heart disease and myocardial ischemia.
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PMID:Connections: heart disease, cellular electrophysiology, and ion channels. 137 69

Hypertrophic obstructive cardiomyopathy is a heart disease characterized by a thickened interventricular septum which narrows the left ventricular outflow tract, and by systolic anterior motion (SAM) of the mitral valve which can contact the septum and create dynamic subaortic obstruction. The most common explanation for SAM has been the Venturi mechanism which postulates that septal hypertrophy, by narrowing the outflow tract, produces high velocities and thus low pressure between the mitral valve and the septum, causing the valve leaflets to move anteriorly. This hypothesis, however, fails to explain why SAM often begins early in systole, when outflow tract velocities are low or negligible or why it may occur in the absence of septal hypertrophy. The goal of this study was therefore to investigate an alternative hypothesis in which structural abnormalities of the papillary muscles act as a primary cause of SAM by altering valve restraint and thereby changing the geometry of the closed mitral apparatus and its relationship to the surrounding flow field. In order to test this hypothesis, an in vitro model of the left ventricle which included an explanted human mitral valve with intact chords and papillary muscle apparatus was constructed. Flow visualization was used to observe the ventricular flow field and the mitral valve geometry. Displacing the papillary muscles anteriorly and closer to each other, as observed clinically in patients with cardiomyopathy and obstruction produced SAM in the absence of septal hypertrophy. Flow could be seen impacting on the upstream (posterior) surface of the leaflets; such flow is capable of producing form drag forces which can initiate and maintain SAM.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Insights from in-vitro flow visualization into the mechanism of systolic anterior motion of the mitral valve in hypertrophic cardiomyopathy under steady flow conditions. 138 19

Cardiomyopathies are defined as 'heart muscle diseases of unknown cause' and classified into hypertrophic, dilated and restrictive types, respectively. Hypertrophic cardiomyopathy is notable for massive ventricular hypertrophy without obvious cause, impaired diastolic and systolic function, a tendency for sudden death and a familial propensity. Dilated cardiomyopathy by contrast, demonstrates severe systolic failure progressing to congestive heart failure, with usually no familial tendency. Restrictive cardiomyopathy and diastolic heart disease represent syndromes with restriction to ventricular filling due to restrictive forces in the endomyocardium (and in constrictive pericarditis in the pericardium). The commonest cause of restrictive cardiomyopathy is endomyocardial fibrosis now usually known as hypereosinophilic endomyocardial disease. Specific heart muscle diseases are those conditions in which myocardial disease is due to a known cause: they usually produce systolic failure though occasionally a restrictive syndrome is evident. Amyloid heart disease occupies a place intermediate between cardiomyopathies and specific heart muscle diseases. The major features of the above conditions are described and current and future advances noted. Examples are the identification of the gene probably responsible for hypertrophic cardiomyopathy located on chromosome 14, and the identification of virus RNA particles in the myocardium in both myocarditis and in dilated cardiomyopathy, which strengthens the growing evidence suggesting that some cases of dilated cardiomyopathy may be due to previous myocarditis.
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PMID:Cardiomyopathies and specific heart muscle diseases. Definitions, terminology, classifications and new and old approaches. 140 13

We report a case of renal cell carcinoma with pulmonary metastases treated with recombinant alpha interferon and subsequently presenting as congestive heart failure due to a dilated cardiomyopathy. A 66-year-old man presented himself to the department of internal medicine at our hospital with a complaint of persistent cough with sputum on August 27, 1988. Ultrasonogram, computed tomography and angiography showed a right renal cell carcinoma and chest x-ray films disclosed bilateral multiple nodular shadows, probably representing metastases of the renal tumor. After being transferred to our department, the patient underwent the ligation of the right renal artery and vein and the postoperative treatment with recombinant alpha interferon, achieving a complete response for pulmonary metastases and a partial response for the primary region. On February 14, 1990 the patient was admitted to our hospital with a complaint of dyspnea to be diagnosed as congestive heart failure due to dilated cardiomyopathy. The interferon therapy was suspected to have caused the heart disease, and four months after discontinuation of interferon therapy the heart failure symptoms had improved, but hypokinesis of the cardiac wall still persisted. To our knowledge, this may be the first case of alpha interferon-related cardiomyopathy in Japan.
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PMID:[Dilated cardiomyopathy following alpha interferon therapy of renal tumor with pulmonary metastases: a case report]. 141 58

In order to determine the results of steroid-sparing maintenance immunosuppression in paediatric patients who have undergone orthotopic heart transplantation (OHT), a retrospective study was undertaken in 12 children and five infants (median age 3.5 years). Preoperative diagnoses were cardiomyopathy in seven and congenital heart disease in 10 patients. Immunosuppression was induced by cyclosporin, azathioprine, methylprednisolone, and antihuman lymphocyte immune globulin. It was maintained with cyclosporin and azathioprine. After induction, five patients received no further steroids. The remainder, except one, required only pulses for rejection (13 episodes or 0.51 episodes/patient year). Long term complications included hypertension in six, and renal impairment in three children. There were no early or late deaths from infection. Actuarial survival was 94% at one year. Of the children followed up for more than one year, all demonstrated an increase in height SD scores (mean (SD) -2.15 (1.35) to -1.15 (1.16)). We conclude that a steroid-sparing maintenance immunosuppression regimen can be successfully employed in paediatric OHT, and that significant catch-up growth can be achieved postoperatively.
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PMID:Paediatric cardiac transplantation with steroid-sparing maintenance immunosuppression. 144 25

All the transplantation units within the Italian Heart Transplantation Project are supported by a section of pathology, devoted to the study of the recipient's heart, to patient monitoring by means of a schedule of endomyocardial biopsies, and, if that was the case, to examine the donor's heart and to analyse the causes of death. When successes and failures of the first five years of the Project's activity are weighed up, good results are observed: of the 847 operations performed (orthotopic, heterotopic and heart-lung transplants, and re-transplants) an actuarial survival rate of 77% at 5 years has been achieved. The sections of pathology believe to have contributed significantly to these results, examining as many as 10,446 endomyocardial biopsies. The indications for transplantation were: dilated cardiomyopathy (48.5%); ischemic (35.3%); valvular (5.9%) and congenital (2.4%) heart disease; hypertrophic cardiomyopathy (2.2%); endocardial fibroelastosis (1.7%); restrictive cardiomyopathy (1.4%); anthracycline cardiotoxicity (0.8%); myocarditis (0.8%); cardiac tumours (0.5%) and arrhythmogenic cardiomyopathy (0.2%). Distribution of recipients by sex and age varied according to the indications for transplantation: males were more common among the patients transplanted for ischemic (97%) and valvular (84%) heart disease, as well as for dilated (82%) and hypertrophic (78%) cardiomyopathy, whereas the opposite was true for endocardial fibroelastosis (males constituting 21%) and cardiac tumours (25%). Mean age at transplantation ranged from 49 years (ischemic heart disease) to 6 years (endocardial fibroelastosis). In the follow-up period, a 17.5% death rate was recorded; the main causes of death were the early failure of the transplanted heart (27 pts), postoperative complications (16), hyperacute rejection (4), acute rejection (18), infections (the singular most frequent cause of death, 35 pts), the proliferative endoarteritis of coronary branches (the so-called chronic rejection, that caused 21 deaths and required 14 re-transplants) and the development of neoplasms (11). The actuarial survival curve drops to 89% after the first postoperative month, abates to 82% at the end of the first year, and progressively decreases to 77% at the end of the fifth follow-up year. Rejection monitoring required an average number of 12.5 endomyocardial biopsies per recipient, and allowed 1.7 rejection episodes per patient to be diagnosed. The fewer were the rejection episodes occurring in a unit, the higher was the percentage of deaths due to infections.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:[The contribution of pathology sections to the Italian Heart Transplant Project in the first 5 years of its activities (1985-1990)]. 147 59

Seven inbred mouse strains were examined for the presence of chronic Chagas' cardiomyopathy in postacute Trypanosoma cruzi infection. DBA/1, DBA/2, BALB/c, B10.T (6R), B10.Q, B10.D2, and B6 mice were infected for 100 days with the Brazil strain of T. cruzi. Standard histologic examination of cardiac tissue from these mice revealed the following relationship among the different strains based on the severity of observed inflammation (myocarditis): BALB/c, DBA/1, and DBA/2 were the most inflamed; B10.T (6R) and B10.Q were intermediate; and B6 and B10.D2 showed the least inflammation. Examination of these tissues for characteristics of myocardiopathy such as cell swelling, edema, vacuolization, necrosis, myocytolysis, connective tissue infiltration, and thinning of the right ventricular wall indicated a relative relationship among the different strains relative to the severity of cardiomyopathy as follows: BALB/c, DBA/2, and DBA/1 showed the most cardiopathy (pathopermissive); B10.T (6R) and B10.Q showed intermediate pathology; and B6 and B10.D2 showed the least involvement (pathoresistant). Anti-heart antibody present in the sera of all these mice showed specific reactivity in western blots to a 43-kDa glycoprotein from normal heart tissue. Also, anti-heart antibody enzyme-linked immunosorbent assay titers for all mouse strains were similar and showed no correlation with the severity of tissue damage. The fact that different inbred strains show various degrees of myocarditis and cardiomyopathy may be useful in the study of pathogenesis of chronic Chagas' disease. Results from this limited list of inbred strains suggest that background genes, rather than the major histocompatibility complex, play the major role in the expression of cardiac pathogenesis.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Differential cardiac histopathology in inbred mouse strains chronically infected with Trypanosoma cruzi. 149 Dec 99

Technetium-99m teboroxime (TEBO) is a new technetium-based myocardial perfusion imaging agent, which has high myocardial extraction and rapid myocardial washout. Its rapid myocardial washout may necessitate rapid imaging protocols. This study was designed to perform exercise/rest SPECT imaging protocols with rapid data acquisition (from 2.8 +/- 1.4 min to 11.2 +/- 4.1 min after injection) in 171 patients with coronary artery disease, 15 patients with cardiomyopathy and 8 patients with other heart disease. The rapid imaging protocols resulted in a high prevalence of good image quality. The diagnostic value of TEBO was recognized from the high concordance of image findings with thallium-201 (201Tl) scintigraphy, 88.2% in the exercise protocol and 89.9% in the rest protocol. Also, the sensitivity and specificity of TEBO for detecting coronary artery disease were comparable (86.6% and 53.9%, respectively) with those of 201Tl (90.7% and 46.2%, respectively). No toxic effects of TEBO were observed in subjective and objective clinical findings and blood examinations. TEBO was finally evaluated to be useful in 98.4% of the patients. Thus, this agent has good clinical potential for myocardial perfusion imaging.
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PMID:[Diagnostic value of a new myocardial perfusion agent, 99mTc-teboroxime (SQ30,217) in patients with coronary artery disease, utilizing a SPECT imaging protocol: a multicenter phase III clinical trial]. 149 86


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