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)

The effect of diltiazem on myocardial ischemia in patients with hypertrophic cardiomyopathy (HCM) was evaluated by exercise myocardial 201Tl single photon emission computed tomography (SPECT). Exercise myocardial SPECT was performed before and 8 weeks after oral administration of diltiazem (180 mg/day) in 20 patients with HCM who showed transient perfusion defects on exercise myocardial 201Tl SPECT under control conditions. SPECT images were divided into 17 segments. The 201Tl perfusion defects were visually scored and evaluated as the defect score. The transient dilation index was calculated as an index of subendocardial ischemia. Improvement of the defect score was demonstrated in 15 patients after the administration of diltiazem. The mean defect score decreased significantly from 9.90 +/- 5.17 to 5.50 +/- 4.89 (p < 0.0001). Although 16 of 20 patients showed an abnormal transient dilation index before diltiazem treatment, 16 showed improvement and 13 of these normalized after diltiazem therapy. The mean transient dilation index decreased from 1.16 +/- 0.10 to 1.02 +/- 0.09 (p < 0.0001). In conclusion, diltiazem prevents or diminishes myocardial ischemia in patients with HCM.
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PMID:Effects of diltiazem on myocardial perfusion abnormalities during exercise in patients with hypertrophic cardiomyopathy. 997 72

A 72-year-old man presented with apical hypertrophic cardiomyopathy followed by midventricular obstruction and apical aneurysm. Doppler echocardiography revealed an abnormal blood flow from the apical aneurysm to the left ventricular outflow through the obstructive lesion during diastole. Myocardial perfusion scintigraphy showed no ischemic change in the apex. This case suggests that apical aneurysm may not be caused by ischemia, although previous reports showed ischemic degeneration or fibrosis may be a cause of an apical aneurysm.
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PMID:[Apical hypertrophic cardiomyopathy followed by midventricular obstruction and apical aneurysm: a case report]. 1022 4

It has been suggested that in hypertrophic cardiomyopathy (HC), vascular abnormalities are not restricted to the heart. Flow-mediated dilation of peripheral conductance arteries (reflecting their endothelial function) has not yet been studied in HC. Our aim was to assess both flow-dependent dilation of the brachial artery and flow responses (dependent on resistance vessels) during forearm reactive hyperemia (RH) in nontreated HC patients. The authors studied 13 HC patients and 14 age- and sex-matched healthy controls. None of them exhibited any factors known to be associated with endothelial dysfunction. Using 7 MHz ultrasound, brachial artery diameter and Doppler flow velocity were measured continuously at baseline and throughout 1 min of RH following 5 min of forearm ischemia induced by inflation of a blood pressure cuff. Arterial diameter and RH flow are expressed as percent changes with respect to the baseline. Flow-dependent dilation was similar in the HC patients and control subjects (7.2 +/- 9.5% vs 9.9 +/- 10.4%, p>0.05). Compared to the control group, RH flow in HC was decreased; however, differences did not reach statistical significance until 60 sec of RH (112 +/- 102% vs 261 +/- 217%, p<0.05; HC vs controls). In HC patients, endothelial function of peripheral conductance arteries is preserved. Hence, a defect in the forearm arterial bed in HC seems to be limited to mechanisms maintaining the dilation of resistance vessels during decreasing RH flow.
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PMID:Impaired response of the forearm resistance but not conductance vessels to reactive hyperemia in hypertrophic cardiomyopathy. 1022 61

Sudden cardiac death due to ventricular arrhythmias remains a significant problem. In most studies about 50% of all death related to coronary artery disease and heart failure are sudden and unexpected and are caused by acute fatal ventricular tachycardia and fibrillation. Most of the patients suffering sudden cardiac death have some kind of structural heart disease but 80% of SCD events are associated with coronary artery disease, 10-15% with dilated and hypertrophic cardiomyopathy, and only small fraction with the less common disorders as valvular heart disease, ventricular dysplasia and cardiac involvement in sarcoidosis or amyloidosis. In some patients the anomaly responsible for sudden cardiac death is not structural but mainly electrical as in patients with the long QT syndrome, WPW syndrome or in patients with a proarrhythmic effect from antiarrhythmic drugs. In this review, data from clinical trials and other studies on on antiarrhythmic therapies have been evaluated in order to determine effective strategies for the prevention sudden cardiac death in high risk patients. Taken together with the mortality data routine prophylactic use of class I antiarrhythmic drugs in the patients survivors of acute myocardial infarction and patients with heart failure is associated with increased risk of death. Conversely beta-blockers are associated with significant reduction in nonfatal cardiac arrest in the short term trials and sudden cardiac death in long term trials. These benefits are likely due to relief ischemia, reduction of heart rate and maintenance favourable autonomic nervous system balance. Overall trial data on amiodarone suggests that this agent is effective in reducing the risk of death in survivors of cardiac arrest, post infarction patients, and patients with heart failure but the routine prophylactic use of amiodarone remains of uncertain efficacy. The physician who considers the use of antiarrhythmic medications in patients with ventricular arrhythmias must be aware of which arrhythmias are malignant or potentially malignant and which are benign and the decision to initiate antiarrhythmic therapy should be based on consideration of the patients absolute mortality risk.
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PMID:[Antiarrhythmic agents in the prevention of sudden cardiac death]. 1036 92

I-123 labeled methyl-branched fatty acid, BMIPP, has been used mainly in Europe and Japan for the evaluation of various cardiac diseases. BMIPP uptake abnormality is usually more prominent tan perfusion, representing discordant BMIPP uptake less than thallium. This finding is observed in various cardiac disease conditions such as acute myocardial infarction, stable and unstable angina, hypertrophic and dilated cardiomyopathies. Many BMIPP studies combined stress thallium imaging in patients with coronary artery disease and hypertrophic cardiomyopathy demonstrated that such discordant BMIPP uptake less than thallium is related to stress-induced ischemia as evidenced by reversible thallium defect after exercise. BMIPP imaging is able to detect metabolic alteration in the heart which is not available by perfusion imaging alone.
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PMID:BMIPP compared with thallium redistribution. 1045 3

Iodinated fatty acid compounds have an important role in early detection of myocardial abnormalities and provide insights into pathological states in the heart. Among them, 15-(p-iodophenyl)-3R,S-methyl pentadecanoic acid (BMIPP) has been most widely used providing excellent images of the left ventricular myocardium due to high myocardial uptake and long retention. The previous chapters have focused on the basic characters and clinical applications of this compound. However, the precise mechanisms of myocardial kinetics should be further investigated under various conditions. Most of the studies showed reduced BMIPP uptake relative to perfusion in a variety of myocardial disorders, whereas an increase in BMIPP uptake relative to perfusion is often reported. The potential mechanisms of such conflicting results are discussed, but basic studies should be performed to clarify such results in detail. There are a number of clinical values of this compound. Since alteration of fatty acid is observed in the repetitive ischemia, BMIPP can be used for detecting severe ischemic episodes. The concept of 'ischemic memory' imaging can be applied for patients with unstable or vasospastic angina at rest and for those with acute myocardial infarction with successful revascularization to identify the risk area. The discordant decrease in BMIPP uptake relative to perfusion is often seen in ischemic but viable myocardium, and therefore, the combined imaging of BMIPP and perfusion can be used for assessment of tissue viability. Furthermore, abnormal BMIPP uptake is most often observed in hypertrophic cardiomyopathy, and thus, this compound can be used for an early detection and differential diagnosis of the cardiomyopathy. Although BMIPP imaging seems to be quite promising in many fields, the number of patient data remain limited. In this respect, a multicenter study with a vast majority of patients is warranted to confirm these important values of BMIPP. In addition, this attractive tracer should be available all over the world to confirm its clinical value in the near future.
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PMID:Future aspects of BMIPP. 1045 6

MRI myocardial tagging is now a well-developed method for evaluation of regional myocardial contraction. A series of progressively more refined imaging strategies, combined with advances in analytic strategies have provided a strong armamentarium of methods. Important insights into normal human physiology of left ventricular systolic and diastolic function have been developed using one-dimensional, two-dimensional and three-dimensional analyses of myocardial deformation. In disease states, improved understanding and detection of early alterations in myocardial function in hypertensive heart disease has been possible. In addition, improved understanding of effects of ischemia and infarction on regional function has been possible. Further, after acute myocardial infarction, clearer definition of the natural history of contractile dysfunction in the infarct region and the zone adjacent to the infarct have been possible. Similarly, effects on regional function of a number of important pharmacologic agents used for treatment, such as angiotensin converting enzyme inhibitors, beta blockers and angiotensin receptor blockers have been characterized. In the cardiomyopathies, myocardial tagging has permitted more reliable assessment of heterogeneity of segmental function, especially in hypertrophic cardiomyopathy. Finally, initial applications of myocardial tagging to assessment of right ventricular regional function in hypertrophied hearts with and without major congenital abnormalities have generated advances in understanding of effects of hypertrophy on right ventricular function.J. Magn. Reson. Imaging 1999;10:609-616.
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PMID:MRI myocardial tagging. 1054 69

The rapid development of nuclear medicine instruments and the widespread availability of new radiopharmaceutical agents has created a new era of nuclear cardiology. This review will introduce new techniques beyond perfusion and function that have recently become available in Japan. Tc-99m perfusion imaging agents provide excellent myocardial perfusion images that may enhance diagnostic accuracy in the study of coronary artery disease. In addition, greater photon flux from the tracer permits simultaneous assessment of regional perfusion and function with the use of first-pass angiography or ECG-gated acquisition. In addition, Tc-99m perfusion agents are available for acute patients in emergency departments. When the tracer is administrated at both the acute and subacute phases of myocardial infarction, perfusion SPECT imaging permits accurate estimates of areas at risk and salvaged myocardium. Nuclear cardiology has progressed toward biochemical imaging in vivo. Positron emission tomography (PET) enables metabolic assessment in vivo. Preserved FDG uptake indicates ischemic but viable myocardium that is likely to improve regional dysfunction after revascularization. While FDG-PET is available only in a limited number of facilities, FDG-SPECT using ultrahigh energy collimators and branched fatty acid analog I-123 BMIPP SPECT offer potential for metabolic imaging in routine clinical settings. Less uptake of BMIPP than thallium is often observed in the ischemic myocardium and hypertrophic cardiomyopathy. Such a perfusion-metabolic mismatch as that in FDG-PET seems to be similarly observed in BMIPP SPECT. Severe ischemia is identified as reduced BMIPP uptake at rest despite normal or normalized perfusion, suggesting a significant role of BMIPP in ischemic memory imaging. I-123 MIBG uptake in the myocardium reflects adrenergic neuronal function in vivo. In the study of coronary artery disease, neuronal denervation is often observed around the infarcted myocardium and post-ischemic region as well. More importantly, reduced MIBG uptake in these patients can assess the severity of congestive heart failure. In addition, the improvement in MIBG can be seen in relation to improved patient condition following medical treatment. These new techniques will provide insights into new pathological states in ischemic heart disease and a variety of myocardial disorders. Nuclear cardiology plays an important role in selecting optimal treatments for these patients.
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PMID:[Progress in nuclear cardiology: new imaging beyond perfusion and function]. 1056 67

The conceptual model of the classical "ischemic cascade" has served cardiologists well for decades. It correctly predicts clinical findings during imaging stress testing in the presence of coronary artery disease or epicardial coronary artery spasm, where perfusion and wall motion abnormalities provide a substantially higher sensitivity than ECG changes. However, empirical experience has taught us that stress-induced ischemic-like ECG changes, often accompanied by perfusion abnormalities, are the rule rather than the exception in pathophysiological conditions during which the occurrence of ischemia usually cannot be proven, characterized by angiographically normal arteries and reduced flow reserve, such as syndrome X, arterial hypertension and hypertrophic cardiomyopathy. These stress-induced "echocardiographically silent" ST segment changes may be associated with impaired coronary flow reserve and systemic endothelial dysfunction. In hypertrophic cardiomyopathy stress-induced ischemic-like ST segment depression is linked to higher long-term incidence of adverse events. It is entirely likely that our monolithic view of ischemia mirrored in the classical ischemic cascade should be integrated by the awareness of the reverse or alternative "ischemic" cascade best describing microvascular disease, with ECG changes coming first, perfusion abnormalities second, and echocardiographic changes usually being absent. Not all forms of myocardial ischemia are the same, and milder, patchy degrees of myocardial ischemia--as those hypothesized, but not proven, in microvascular angina--remain silent in its mechanical functional manifestations and may well represent a physiological scotoma of stress echocardiography. "Anatomic lies" on the ECG may be overturned into "physiologic truths" when coronary flow reserve or systemic endothelial function is considered.
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PMID:The alternative "ischemic" cascade in coronary microvascular disease. 1060 88

It has been presented a case of an eleven-year-old patient admitted with a pattern of ventricular fibrillation and diagnosed as hypertrophic cardiomyopathy. Admission analysis and myocardia anatomy evolution suggested ischemic etiology. We checked the risk factors of sudden death, its relation with ischemic disease and the etiology of ischemia in the hypertrophic myocardiopathy.
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PMID:[Sudden death and ventricular fibrillation of possible ischemic origin in a boy with hypertrophic myocardiopathy]. 1073 61


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