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Query: UMLS:C0022116 (ischemia)
 91,303 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We encountered a patient with hypertrophic cardiomyopathy complicated with exercise-induced myocardial ischemia. Exercise-stress 99mTc-tetrofosmin imaging demonstrated reversible ischemia in the lateral wall, whereas resting fatty acid imaging with a new beta-methyl branched fatty acid analogue, I-123-15-(p-iodophenyl)-9-(R,S)-methylpentadecanoic acid (123I-9-MPA), showed impaired uptake and accelerated washout kinetics in the inferoapical and posteroseptal walls but not in the ischemia-related region. These findings suggest that the metabolic derangement is closely related to cardiomyopathy per se rather than exercise-induced myocardial ischemia in this patient with hypertrophic cardiomyopathy and a spastic coronary lesion so that myocardial perfusion and 123I-9-MPA imagings may contribute to clarifying the etiological background of impaired myocardial fatty acid metabolism.
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PMID:Impaired myocardial accumulation of 15-(p-iodophenyl)-9-(R,S)-methylpentadecanoic acid in a patient with hypertrophic cardiomyopathy and exercise-induced ischemia due to vasospasm. 1077 May 82

Nuclear medicine techniques have been applied to cardiomyopathy as well as in ischemic heart diseases. Various types of radiopharmaceutical including 201Tl and 99mTc-labeled perfusion tracers, 123I-labeled fatty acid(BMIPP), sympathetic function (MIBG) and tracers for myocardial injuries have been used. Perfusion imaging identifies stress-induced ischemia associated with myocardial damage. Recent application of gated SPECT enables simultaneous assessment of ventricular function. 123I-BMIPP and MIBG can detect metabolic abnormality, which has diagnostic and prognostic value for hypertrophic cardiomyopathy. The MIBG uptake index, heart-to-mediastinum ratio, is known to show good prognostic value for estimating dilated cardiomyopathy. Nuclear medicine plays unique roles for evaluating functional and metabolic derangement in cardiomyopathy.
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PMID:[Nuclear medicine imaging for cardiomyopathy]. 1088 87

Cardiac hypertrophy or hypertrophy of cardiomyocytes is an adaptive response of the heart against an intrinsic or extrinsic damage in cardiomyocytes. A typical intrinsic defect causing cardiac hypertrophy is the sarcomere mutations found in hypertrophic cardiomyopathy (HCM) and extrinsic defects include cardiac ischemia, pressure- or volume-overload, metabolic diseases and arrhythmias. The hypertrophic response is a compensatory mechanism to augments cardiac output, however, sustained hypertrophy may lead to systolic dysfunction or de-compensation state. It is well known that some patients with HCM develop to dilated-phase or burn-out phase, which resembles dilated cardiomyopathy (DCM). In this review, molecular mechanisms underlying the cardiac hypertrophy in HCM and DCM will be discussed.
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PMID:[Molecular aspects of cardiac hypertrophy and their implications in cardiomyopathies]. 1088 18

Early treatment of acute myocardial infarction (AMI) can improve the rate of coronary patency, salvage myocardium, and ultimately save lives; thus, rapid recognition of patients at a higher risk of developing AMI is very important. The clinical history in patients with documented AMI is sometimes atypical, and the initial cardiac enzyme levels often are within the normal range. Moreover, the typical ST-segment elevation is often absent on the initial electrocardiogram in patients who subsequently sustain an AMI. Stress-induced segmental wall motion abnormalities (SWMAs) in coronary artery disease patients can be readily detected by conventional two-dimensional echocardiography. Moreover, echocardiography is the only technique available that allows real-time assessment of stress-induced reduction in systolic wall thickening, a highly specific sign of myocardial ischemia. Echocardiography for the diagnosis of acute ischemia is most helpful in subjects with a high clinical suspicion but nondiagnostic electrocardiograms. Under these circumstances, reversible SWMA confirms the diagnosis of acute coronary syndrome. The location of regional SWMAs correlates well with the distribution of the artery involved and pathological evidence of infarction. A trained eye can easily recognize cardiac causes of acute chest pain other than coronary diseases such as aortic stenosis, hypertrophic cardiomyopathy, mitral valve prolapse, pericarditis, and aortic dissection. When echocardiography is performed soon after the patients arrival at the emergency department (ED) or during a chest pain episode, SWMAs are detected in 90-95% of transmural infarctions and in 80-90% of nontransmural or subendocardial infarctions, and the specificity of echocardiography is approximately 80-90%. Although stress echocardiography performed in the ED and interpreted at a distance through the use of telemedicine has the potential of being convenient, in our opinion, any form of stress echocardiography should be performed in the echocardiography laboratory only after an AMI has been completely ruled out. The detection of jeopardized myocardium early after AMI can identify patients at a higher risk to develop subsequent events. In conclusion, echocardiography is cost effective in the triage of patients presenting with acute chest pain when performed soon after ED admission or during a chest pain episode. However, echocardiography must be readily available, expeditiously performed, and skillfully interpreted. The clinical use of stress echocardiography in acute coronary syndromes has been greatly improved with the introduction of digital and second harmonics technology and further enhanced by the availability of contrast agents.
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PMID:Diagnostic and prognostic use of stress echo in acute coronary syndromes including emergency department imaging. 1097 25

The mechanism underlying cardiac arrest in patients with hypertrophic cardiomyopathy (HC) is intriguing. In the clinical setting, myocardial ischemia has long been incriminated, particularly in the young. Among 274 cardiovascular sudden deaths in the young (< or = 35 years), 19 (7.0%), 14 males and 5 females, median age 23 years, had HC. Familial occurrence of HC was ascertained in 3 (16%). SD occurred on effort in 6 (31%). Previous syncope occurred in 5 and palpitations in 3. Basal electrocardiogram (ECG) was abnormal in 7 of 8 available cases. Hypertrophy was septal asymmetric in 14. Gross examination showed large isolated or multiple septal scars in 11 (58%); at histomorphometry, the mean percent area of fibrosis of the septal myocardium was 18.6 +/- 6. Four showed a deep intramyocardial course of the left anterior descending coronary artery. At histology, myocardial disarray involved 30 +/- 16% of the septal myocardium; evidence of acute-subacute myocardial necrosis was present in 14 (74%), 1 of them with a regional acute myocardial infarction. By comparing hearts with (n = 11) and without (n = 8) areas of scar-type fibrosis, we found a statistically significant difference in terms of age (25.5 +/- 5.4 v 15.5 +/- 12.4 years, P = .04), septal thickness (25.4 +/- 5.4 v 15.4 +/- 4.9 mm, P < .001), percent increase of septal thickness versus normal value for age and sex (46.2 +/- 15 v 25.2 +/- 13.6%, P < .01) and mean score of small vessel disease (1.7 +/- 0.4 v 1.2 +/- 0.4, P = .04). Linear regression analysis showed a positive correlation of percent area of replacement fibrosis with septal thickness (P = .01) and with mean score of small vessel disease (P < .01). In conclusion, our pathologic findings of ischemic damage, either acute-subacute or in the form of fibrotic scars, support the clinical evidence that ischemia occurs in the natural history of HC and may contribute to life-threatening electrical instability.
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PMID:Hypertrophic cardiomyopathy and sudden death in the young: pathologic evidence of myocardial ischemia. 1098 48

Sudden unexpected death, often occurring in young asymptomatic patients, is the most devastating facet of the natural history of hypertrophic cardiomyopathy (HCM). It appears to be the consequence of primary ventricular tachyarrhythmias arising in an electrically unstable myocardial substrate characterized by disorganized cellular architecture, ischemia, cell death, and replacement scarring. Although identification of the HCM patient subset at high risk for a catastrophic event with precision continues to present challenges, treatment strategies for the prevention of sudden death are now available. In particular, the implantable cardioverter-defibrillator has a high degree of efficacy in sensing and terminating potentially lethal ventricular tachyarrhythmias and a life-saving role in both the primary and secondary prevention of sudden cardiac death in HCM.
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PMID:Ventricular arrhythmias, sudden death, and prevention in patients with hypertrophic cardiomyopathy. 1106 May 79

The echocardiographic examination is generally performed in patients with heart failure and it often gives a significant contribution to the differential diagnosis. Firstly, the evaluation of left ventricular pump function by measuring the ejection fraction (EF) can distinguish patients with heart failure into two different groups, with depressed or preserved EF. The most frequent causes of heart failure and depressed EF are coronary artery disease, idiopathic dilated cardiomyopathy (DCM) and hypertensive heart disease. Although the echocardiographic features of coronary artery disease versus idiopathic DCM may be similar, the demonstration of inducible ischemia at dobutamine echocardiographic test suggests the presence of significant coronary artery disease and may be useful in the selection of cases for coronary arteriography. The association of left ventricular hypertrophy, hypokinesis and, sometimes, significant dilation is compatible with hypertensive heart disease or end-stage hypertrophic cardiomyopathy. No useful echocardiographic findings can identify the patients with genetic DCM or affected by myocarditis from other cases with idiopathic DCM. Some advanced cases of right ventricular dysplasia/cardiomyopathy may show a biventricular involvement and mimic DCM; these patients are usually characterized at echo by predominant right ventricular dilation and multiple a-dyskinetic bulges in the absence of pulmonary hypertension. Very difficult to manage are the patients with significant left ventricular dysfunction and severe valvular heart disease (such as aortic stenosis or mitral regurgitation). According to the literature, the left ventricular systolic function is relatively preserved (EF > 40%) in 30-40% of patients with heart failure. In these cases a diastolic dysfunction may be hypothesized. Echo-Doppler evaluation can be helpful in the recognition of signs of increased left ventricular stiffness ("restrictive filling pattern") and of increased filling pressures. In the differential diagnosis one must first consider the most frequent heart disorders that may present with this clinical syndrome, coronary artery disease and hypertensive heart disease. Furthermore, other less common diseases characterized by heart failure due to predominant diastolic dysfunction are the following: hypertrophic and restrictive cardiomyopathies, infiltrative heart diseases, such as amyloidosis, and constrictive pericarditis. Restrictive cardiomyopathy is characterized by heart failure and preserved left ventricular EF in the absence of significant ventricular dilation and hypertrophy; typical, although not pathognomonic, echocardiographic features are atrial enlargement ad restrictive filling pattern. In distinguishing constrictive pericarditis from restrictive cardiomyopathy useful Doppler signs are the wide respiratory variability in flow velocities at mitral and tricuspid levels, due to increased ventricular interdependence caused by the presence of an abnormally rigid pericardium.
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PMID:[Contribution of echocardiography to the diagnosis of patients with chronic heart failure]. 1106 13

Systolic anterior motion of the mitral valve (MV) with dynamic left ventricular (LV) outflow tract obstruction is a well known phenomenon in hypertrophic cardiomyopathy, or other forms of hyperdynamic LV function associated with hypovolemic states, or LV hypertrophy. We report three patients with MV prolapse in the absence of the above predisposing factors, who developed an LV outflow dynamic gradient during acute transient myocardial ischemia. An interaction between structural abnormalities of the mitral apparatus and ischemia-dependent LV shape deformity most likely accounted for the outflow gradient.
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PMID:Dynamic Left Ventricular Outflow Tract Obstruction During Myocardial Ischemia in Mitral Valve Prolapse Syndrome. 1117 71

We searched the medical literature for articles containing markers of cardiac ischemia and echocardiography in the evaluation of patients presenting to the emergency department to determine their combined clinical use. Several published articles indicate two-dimensional echocardiography is a useful and cost-effective imaging technique for the evaluation of patients with chest pain in the emergency department. New studies are emerging that evaluate ischemic markers in combination with echocardiography to assess patients presenting to the emergency department with chest pain. We searched the MEDLINE Database for English-language articles published from December 1980 to August 1998 using the key words troponin, echocardiography, myocardial infarction, and emergency. These key words were crossed referenced to determine publications in this area. Pertinent trials and reviews were selected from the database. There were six articles evaluating biochemical markers of ischemia and echocardiography to assess patients presenting with acute coronary syndromes in the emergency department. Very few studies combined the information obtained from novel ischemic markers and echocardiogram analysis to help delineate potential cardiac etiologies of acute coronary syndromes. However, the limited studies available indicate that echocardiography is both sensitive and specific for detecting acute myocardial infarction. The presence of regional wall motion abnormalities increases the chance of in-hospital complications and likelihood of developing congestive heart failure after admission for unstable angina. The combined use of troponin T levels and echocardiographic imaging was a more powerful predictor of adverse events than were isolated results. Myocardial scarring with ventricular wall thinning or aneurysm may allow for rapid diagnosis of 'occult' coronary artery disease in a patient presenting with chest pain who does not have a previous history of a cardiovascular event. Echocardiography may also help identify other cardiovascular causes of chest pain, such as aortic dissection, aortic stenosis, cardiac tamponade, pericarditis, and hypertrophic cardiomyopathy. The clinical use of combining ischemic markers of disease with echocardiographic imaging seems justified given their unique clinical advantages. Future clinical trials are needed to determine whether the combination of novel ischemic markers and echocardiography can provide for a more expedient and accurate diagnosis, resulting in improved patient care and a safe reduction in unnecessary hospitalization.
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PMID:Clinical Use of Ischemic Markers and Echocardiography in the Emergency Department. 1117 40

An 11-year-old patient with diagnosis of hypertrophic cardiomyopathy (HCM) developed marked elevation of troponin I in the absence of electrocardiographic signs of ischemia after two episodes of supraventricular tachycardia. At follow-up the level of troponin I returned to normal. The role of troponin I in patients with HCM as a risk marker deserves further evaluation.
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PMID:Troponin I elevation after supraventricular tachycardia in a child with hypertrophic cardiomyopathy. 1117 73


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