Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0018799 (heart disease)
 34,133 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Problems of arrhythmogenic sudden death (ASD) in athletes have been re-assessed on the clinicopathological plane, encompassing the emerging, unsolved, question of so-called idiopathic ventricular tachycardia, and its debated diagnostics versus arrhythmogenic right ventricular dysplasia-cardiopathy. Ischemic-infarction ASD from coronary artery pathology in young athletes has been seen to present with atherosclerotic "soft" subintimal plaques, rich in newly formed smooth myocytes, often attended by adventitial mast cell, as suspect microscopic markers of spasm, relevant to reperfusion; these features can be found also in precociously intramural arteries, responsible for ASD. Rare congenital abnormalities of the coronary ostia occasionally underlie ASD, together with the acquired aneurysmic coronaritis of chronic Kawasaki disease. Ischemic ASD can also be due to coronary arteriolopathy attending hypertrophic cardiomyopathy, a not uncommon disease in athletes, to be carefully discriminated from training heart hypertrophy. Young South-American sportsmen with Chagas' chronic cardiopathy seem to be at particular risk of ASD. Minor, but specific arrhythmogenic cardiac malformations such as accessory AV pathways have been detected in athletes succumbing to otherwise unexplained ASD, undergone careful post-mortem investigation. The need of more attentive and extended histopathologic control emerges from the hitherto ignored cardiac neuropathological substrates of reflexogenic ASD, which is cogent to problems of ASD in competing athletes. The thorough examination of the cardiac vascular centers in the brain stem, and of the peripheral cardiac innervation, at either abutments of the arc of dive- and/or Bezold-Jarisch cardioinhibitory-vasodepressor reflex, made it possible to suggest novel clinicopathological explanations in controversial cases of athletes' ASD, safeguarding from grave leval misjudgements due to sport's forensic medical mistakes.
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PMID:Structural and non-structural disease underlying high-risk cardiac arrhythmias relevant to sports medicine. 750 Jun 31

Pheochromocytoma is the most frequent cause of adrenal sudden death, which is the unique sign in 1.5% of cases. After a short review of the literature, we report a case of a 36 years old asymptomatic woman, who died suddenly and unexpectedly while receiving preoperative treatment. Gross examination did not allow to reveal any cause of death. Microscopy revealed signs of acute myocardial ischemia, in the lack of any coronary and catecholaminic heart disease. Azan-Mallory trichromic stain was found to be necessary in revealing myocardial lesions. A plausible death pathway is the following: a single catecholaminic peak might have induced myocardic vessel spasm, which in turn could be responsible for a lethal arrhythmia; the dramatic pressure drop can be the effect of pump failure or of a paradoxical disproportionate beta stimulation.
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PMID:[Pheochromocytoma and sudden death: a case of hyperacute myocardial ischemia]. 761 1

Acute colonic ischemia is the most common form of intestinal ischemia. Nonocclusive ischemic colitis contributes to some of these disorders. Heart disease, such as congestive heart failure, myocardial infarction, arrhythmias, aortic valve disease, and atherosclerotic cardiovascular disease, account for many of its risk factors. The majority of cases are associated with severe congestive heart failure with low cardiac output, or disease states resulting in dehydration, or the splanchnic vasoconstrictive effect of some medications. Reactive splanchnic vasoconstriction is responsible for nonocclusive ischemic colitis. Ischemic colitis induced by a cleansing enema has been reported once before. The authors present a case of coronary artery disease complicated by colonic ischemia following glycerin enema in preparation for coronary bypass surgery. Reactive inferior mesenteric artery spasm in response to the enema was noted in this case, rather than diffuse mesenteric artery spasm in response to low cardiac output state and vasoconstrictive drugs.
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PMID:Nonocclusive ischemic colitis following glycerin enema in a patient with coronary artery disease. A case report. 763 24

Myocardial infarction and sudden cardiac death may be initiated by a sudden intense localized contraction of coronary artery smooth muscle. When this event occurs around a vulnerable eccentric lipid-filled plaque, rupture and extrusion of plaque contents and exposure of collagen occur. This may sometimes be a silent and self-limiting event; other times it leads to thrombus formation. A second wave of spasm due to accumulated platelet and inflammatory mediators may compound the contractile consequences of the initiating event. Spasm involves intrinsic smooth muscle cell electrical mechanisms, hyper-responsive cells, and multiple agonists that synergize their actions, and the involvement of each mechanism varies at different times in the sequence of vascular occlusion. Study of spasm requires vascular systems that adequately model coronary artery responses of the ageing human heart. As previously emphasized, tissues obtained postmortem, and when possible from recipients during heart transplants, must be integral to theory building, alongside animal models, despite the experimental limitations such tissues impose. A multidisciplinary approach, at all levels of vascular physiology and pharmacology, will be necessary to understand coronary motor activity and human heart disease.
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PMID:Coronary artery spasm. Multiple causes and multiple roles in heart disease. 774 58

The association between Friedreich's ataxia and heart disease is well known. Microvascular disease and spasm of coronary arteries have been reported. We report now a patient with the association between this disease and acute myocardial infarction, which raises the hypothesis that it may be related with the already known cardiac abnormalities in this disease.
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PMID:[Acute myocardial infarct and Friedreich's disease]. 788 66

We present three patients without significant coronary or other structural heart disease who were resuscitated after ventricular fibrillation attributed to coronary spasm. Angina pectoris was present in two of the cases and silent myocardial ischemia in the third. All patients were given calcium antagonists at discharge. A defibrillator was also implanted in the patient with silent myocardial ischemia because further episodes of ischemia would probably have occurred without premonitory symptoms. Coronary spasm might be a mechanism of ventricular fibrillation in patients without significant structural heart disease. Diagnostic tests should therefore be performed to confirm or exclude coronary spasm in such cases. The implantation of an automatic defibrillator seems justified in selected patients with documented coronary spasm, silent myocardial ischemia, and associated sustained ventricular tachyarrhythmia, although prospective studies are not yet available.
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PMID:Ventricular fibrillation related to coronary spasm in patients without significant coronary or other structural heart disease. 804 79

To evaluate the prevalence of type I silent myocardial ischemia and silent myocardial infarction, 4,842 men aged 40 to 59 years, identified in occupational samples in Florence and Rome, and free from major heart disease, severe illnesses and chest pain, underwent a 3-stage diagnostic procedure. The first stage included resting electrocardiogram, hyperventilation test, exercise electrocardiogram and 24-hour Holter electrocardiogram. The subjects who were suspected of having type 1 silent myocardial ischemia or previous silent infarction at the first stage (n = 439; 9.1%) were entered into the second stage, which included echocardiogram, thallium 201 scintigraphy in conjunction with exercise testing or dipyridamole test, exercise radionuclide ventriculography and ergonovine test. Three hundred eighty-seven men participated in the second stage; after the diagnostic procedures were performed, 104 men (2.1%) were still suspected of having type 1 silent myocardial ischemia or infarction on the basis of predefined criteria. Sixty-two men continued on into the third diagnostic workup including coronary angiography. The final diagnosis of type 1 silent myocardial ischemia or infarction was reached in 25 patients (prevalence 0.52%; adjusted estimate 0.89%). Of these 25, 19 had coronary atherosclerotic disease, 1 had Kawasaki disease, 1 had coronary anomaly, 1 had induced focal coronary spasm, and 2 had normal coronary arteriograms despite the presence of unquestionable old myocardial infarction. Altogether, 6 patients with silent myocardial infarction were identified.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Epidemiology of silent myocardial ischemia in asymptomatic middle-aged men (the ECCIS Project). 825 31

Long-term follow-up studies of patients with suspected viral myocarditis reveal progression to dilated cardiomyopathy (DCM) in a significant number of cases. Thus, an underlying viral etiology has been hypothesized in the pathogenesis of ongoing heart disease that leads to DCM. Recent application of molecular biology in clinical diagnosis has strengthened this hypothesis. By use of probe hybridization and polymerase chain reaction, enteroviral RNA has been detected in the myocardium of patients at all stages of the disease process: myocarditis, chronic heart disease, and DCM. Experimental murine models of enterovirus-induced heart disease provide a framework for examining the pathogenic mechanisms. Viral cytotoxicity, immunological responses, viral RNA persistence, and spasm of the coronary microvasculature are all implicated in the ongoing disease process. Abnormal cardiac function and heart failure are attributed to the pathological changes that occur.
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PMID:Viral infection and the pathogenesis of dilated cardiomyopathy. 829 57

Self-terminating ventricular fibrillation was recorded in a 47 year old woman without coronary artery or other structural heart disease. Reperfusion was thought to be responsible for the ventricular fibrillation because the arrhythmia started while the ST segment was returning to the baseline during an episode of silent ischaemia that was probably caused by coronary spasm. This case shows that potentially lethal arrhythmias can arise during reperfusion and that ventricular fibrillation during reperfusion may be self-terminating.
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PMID:A patient in whom self-terminating ventricular fibrillation was a manifestation of myocardial reperfusion. 828 May 35

Toxic manifestations of digitalis are one of the most prevalent adverse drug reactions encountered in clinical practice. The estimated incidence is about 20% in hospitalized patients in the USA. The authors describe a rare case of myocardial "catecholamine necrosis" (anteroseptal myocardial infarction) during accidental digitalis intoxication. A male patient, 75 years old, suffering from cirrhosis and ascites, take on by mistake a tablet of digoxin 0.25 mg. four times at day for eleven days. He hadn't heart disease in the past. At the eleventh day the patient showed a deep tiredness and so he was submitted to a clinical examination and electrocardiogram. The ECG demonstrated an anteroseptal myocardial infarction in the second-third electrical stage. The patient was hospitalized. The successive examination revealed: very high plasma digitalis concentrations; an increase of the serum levels of CPK and LDH; a significant increase of plasmatic and urinary catecholamine levels which return to normal values after fifteen days; apical akinesia at the echocardiographic examination; no signs of residual myocardial ischemia to the echo-dypiridamole stress test; normal coronary artery to the coronary arteriography and absence of coronary artery spasm to the ergonovine test. Furthermore the abdominal echography and the abdominal computerized tomography didn't reveal surrenal disease but showed an important liver disease. The patient was free from other cardiac events in the follow-up. Generally, during the digitalis intoxication we observe various rhythm and conduction disturbances. Instead in this case no serious arrhythmias were registered and the main expression of the drug toxicity was an anteroseptal myocardial infarction with undamaged coronary artery. Also the usual extracardiac symptoms and signs of the digitalis intoxication were absent in this case. All these observations can be explained with the pathological increase of the cathecholamine levels, indirectly induced by digitalis; with the direct toxic effect of the drug at the myocardic level; with the contemporary absence of ionic disturbances; with the concomitant liver disease. The direct toxic effect of the digitalis produced an increase in calcium ions availability for the electromechanical coupling and an increase of the intramyocardial pressure; the increase of the adrenergic activity determined contemporary an increase in the oxygen consumption of the myocardial cells, a rise of vascular tone and coronary artery tone and a reduction of the duration of the diastole. All these factors provoked a "primary and secondary" ischemia which evolved toward a real "cathecholamine necrosis" and produced a myocardial infarction. This hypothesis explains the myocardial infarction in absence of injury at the coronary arteriography and without coronary spasm at the ergonovine test; moreover it explains the transient increase in cathecholamine plasma levels observed in the acute phases an normalized after fifteen days. The "cathecholamine necrosis" is an anatomical definition, nevertheless in our opinion it gives account of the rare clinical situation observed.
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PMID:[An unusual case of "catecholamine necrosis" caused by accidental digitalis poisoning]. 855 67


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