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)

Effect of verapamil on myocardial ischemia in patients with hypertrophic cardiomyopathy (HCM) was evaluated by exercise stress myocardial 201Tl SPECT (EX-Tl). EX-Tl were performed before and after 8.8 weeks of oral verapamil (240 mg/day) in 12 patients with HCM who showed transient 201Tl perfusion defects under control conditions. 201Tl perfusion defect was visually scored and judged for 4 grades as normal (0), mild defect (1), moderate defect (2), and severe defect (3). Transient Dilation Index (TDI) was calculated as an index of subendocardial ischemia. Improvements of defect score were demonstrated in 10 patients after administration of verapamil. Two patients showed no change of defect score. Mean defect score decreased significantly from 5.50 to 3.03 (p < 0.001). Although 11 of 12 patients showed abnormal TDI under control conditions, 10 of them revealed improvements of TDI and 7 of those 10 patients disclosed normal TDI after verapamil. Mean TDI decreased from 1.263 to 1.090 significantly (p < 0.01). In conclusion, verapamil may improve myocardial ischemia in patients with HCM.
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PMID:[Effect of verapamil on myocardial ischemia in patients with hypertrophic cardiomyopathy: evaluation by exercise 201Tl SPECT]. 845 43

A male patient presented with symptoms of angor under effort. Echocardiography and angiocardiography revealed apical hypertrophic myocardiopathy, associated with multiple fistulas connecting the anterior descending coronary artery and right coronary artery with the cavity of the left ventricle, as demonstrated by coronariography. We comment on the hypothesis that support a causal relationship between the two anomalies, microfistulas being the possible cause of the reactive hypertrophy through the induction of a coronary steal phenomenon with local ischemia; alternatively, the myocardiopathy itself might be the cause of microfistulas formation by inducing an anomaly in the Thebesius venous system. A pathogenic relationship is suggested between the syndrome of angor and these two rare pathological entities.
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PMID:[Apical hypertrophic myocardiopathy and multiple fistulae between the coronary vessels and the left ventricle]. 853 48

The two left ventricular (LV) papillary muscles are small structures but are vital to mitral valve competence. Partial or complete rupture, complicating acute myocardial infarction, causes severe or even catastrophic mitral regurgitation, potentially correctable by surgery. Papillary muscle dysfunction is a controversial topic in that the role of the papillary muscle itself, in causing mitral regurgitation post infarction, has been seriously questioned; it is less confusing if this syndrome is attributed not only to papillary muscle but also to adjacent LV wall ischemia or infarction. Papillary muscle calcification is easily and frequently detected on echocardiography, but its clinical significance remains uncertain. Papillary muscle hypertrophy accompanies LV hypertrophy of varied etiology and may have a significant role in producing dynamic late-systolic intra-LV obstruction in hypertrophic cardiomyopathy and other hyperdynamic hypertrophied LV chambers. All the above abnormalities can be adequately assessed by 2-D echocardiography and the Doppler modalities. In selected cases, transesophageal echocardiography can provide additional valuable data by improving visualization of papillary muscles and mitral apparatus.
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PMID:The vital role of papillary muscles in mitral and ventricular function: echocardiographic insights. 913 87

Approximately 8 million patients at risk for coronary artery disease undergo noncardiac surgery annually in the United States. This study defined the appropriateness and cost of evaluating these patients with stress imaging tests. Before noncardiac surgery, 178 consecutive patients were prospectively studied by stress imaging. Pretest cardiac risk (low, intermediate, high) was established by interviewing the referring physician and separately by a cardiologist on the basis of the nature of noncardiac surgery and Eagle's clinical criteria. Patients were followed-up for alterations in management and perioperative events until hospital discharge. Referring physicians and cardiologists identified low risk in 24% and 54% of patients, respectively (p < 0.0001). Of 96 patients identified as low risk by cardiologists, 75 had minor surgery and 21 had major surgery, but no clinical risk factors. In the remaining 82 patients with major surgery, ischemia and other severe abnormalities were detected in 19 (23%) patients. At follow-up, no perioperative complications occurred in minor surgery; one patient with major surgery but no clinical risk factors died from complications related to hypertrophic cardiomyopathy. Patients with at least one clinical risk factor undergoing major surgery but who did not have ischemia on stress testing (n = 63) had two complications (infarction and unstable angina). Intervention (revascularization and surgical cancellation) was probably the explanation for the absence of events in 19 patients with ischemia. With a weighted mean Medicare reimbursement ($386), the use of a simple selection algorithm based on noncardiac surgery and clinical risk to avoid testing low-risk patients would have an average cost of $214 per patient, representing a 45% savings.
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PMID:Outcomes and cost implications of a clinical-based algorithm to guide the discriminate use of stress imaging before noncardiac surgery. 926 87

We have recently developed a porcine model with naturally occurring hypertrophic cardiomyopathy (HCM). Similar to humans, occluded intramural coronary artery and damaged mitochondria are frequently observed in these animals in which the disease is thought to be associated with the local ischemia of myocardium. In view of antioxidant functions involved in the ischemic injury, we measured the expression of endogenous antioxidant enzymes in the tissues with and without HCM. The results showed a significant increase of Cu,Zn-superoxide dismutase (SOD), but not Mn-SOD, and decrease of catalase (CAT) activities in the various areas of HCM hearts. It was demonstrated that SOD/CAT ratios in the HCM hearts were significantly higher than those in normals and were found to be dramatically correlated with the severity of cardiac hypertrophy. The altered SOD/CAT ratio was also consistent with increase in lipid damage. We hypothesize that the elevated SOD combined with an inadequate amount of H2O2 scavenging enzyme may lead HCM heart at oxidative stress risk. However, the pathogenic role of imbalanced antioxidant enzyme needs to be further explored.
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PMID:Alteration of endogenous antioxidant enzymes in naturally occurring hypertrophic cardiomyopathy. 944 21

We report a case of hypertrophic cardiomyopathy (HCM) with apical left ventricular aneurysm, which is difficult to review because cases are so rare. A 54-year-old Japanese man was first found to have an electrocardiographic abnormality (T-wave inversion at rest) 19 years ago, and non-obstructive apical HCM without identifiable cause was diagnosed by echocardiography, left ventriculography, and clinical findings. After 19 years, he was admitted because of repeated episodes of palpitation and chest oppression at rest. Widespread left ventricular hypertrophy from the anteroseptal wall to the apex with an apical left ventricular aneurysm was detected by echocardiography, left ventriculography, and cardiac magnetic resonance imaging. Histologic examination of the hypertrophic apical myocardium surrounding the aneurysm showed that the myocardial tissue had been extensively replaced by fibrous tissue containing hypertrophic myocardial fibers, and uptakes of [123I]-metaiodobenzyl guanidine (MIBG) and [123I-] beta-methyliodophenyl pentadecanoic acid (BMIPP) in single-photon emission photography images were reduced despite high myocardial perfusion. On the other hand, histologic examination of the hypertrophic anterior wall revealed myocardial hypertrophy with disorganization; myocardial perfusion and the uptakes of MIBG and BMIPP were preserved. Abnormalities of myocardial fatty acid metabolism and sympathetic neuron activity with preserved perfusion flow and histologic changes such as fibrosis in the apical wall are indicative of apical myocardial injury or ischemia (infarction) without coronary artery stenosis; apical aneurysm may have occurred in severe apical HCM with cavity obliteration up to the midventricular level.
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PMID:Hypertrophic cardiomyopathy with apical left ventricular aneurysm. 955 32

Reversible thallium-201 (201Tl) abnormalities during exercise stress have been used as markers of myocardial ischemia in hypertrophic cardiomyopathy (HCM) and are most likely to identify relatively underperfused myocardium. Although metabolic abnormalities in HCM were reported, the relationship between impaired energy metabolism and exercise-induced ischemia has not been fully elucidated as yet. To assess the relationship between myocardial perfusion abnormalities and fatty acid metabolic abnormalities, 28 patients with HCM underwent exercise 201Tl and rest 123I-15-(p-iodophenyl)-3-methyl pentadecanoic acid (BMIPP) scintigraphy. Perfusion abnormalities were observed by exercise 201Tl in 19/28 patients with HCM. 123I-BMIPP uptake was decreased compared with delayed 201Tl in 106/364 (29%) of the total myocardial segments (p<0.01, McNemar symmetry test). Such disparity between 123I-BMIPP and 201Tl was observed more often in the 49/75 (65%) segments with reversible exercise 201Tl defects (p<0.001). Our results indicate that exercise-induced myocardial ischemia exists in HCM, resulting in metabolic abnormalities. The combination of 123I BMIPP and 201Tl suggests that myocardial ischemia may play an important role in metabolic abnormalities in HCM.
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PMID:Myocardial metabolic abnormalities in hypertrophic cardiomyopathy assessed by iodine-123-labeled beta-methyl-branched fatty acid myocardial scintigraphy and its relation to exercise-induced ischemia. 958 41

We report two patients with out-of-hospital cardiac arrest who recovered after hypothermia therapy. A 25-year-old man and a 16-year-old boy were transferred to our hospital after cardiopulmonary arrest due to idiopathic ventricular fibrillation and hypertrophic cardiomyopathy, respectively. We carried out hypothermia therapy using cooling blankets, and the patients were maintained at 32-33 degrees C for 96 and 36 h, respectively. After slow rewarming, they regained consciousness and recovered. During hypothermia, hypokalemia and arrhythmia occurred. Their arrest times (no spontaneous circulation and no CPR) were 10 min and 8 min, and CPR times (no spontaneous circulation while CPR was being performed) were 24 min and 20 min, respectively. In cases where the duration of ischemia is prolonged, the prognosis is expected to be poor. Therefore, we believe that hypothermia therapy is beneficial for such patients.
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PMID:[Recovery from out-of-hospital cardiac arrest after mild hypothermia: report of two cases]. 969 97

Assessment of regional left ventricular (LV) function in patients with asymmetric LV hypertrophy is difficult with two-dimensional echocardiography mainly because of factors such as LV geometry, structure, regional wall stress, and ischemia. Multiplane transesophageal echocardiography with three-dimensional reconstruction of cross-sectional images was used for quantitative evaluation of regional wall thickness and fractional thickening. Fifteen patients (56 +/- 13 years old) with hypertrophic cardiomyopathy (LV ejection fraction 71% +/- 4%), 15 (62 +/- 13 years) with hypertensive heart disease (ejection fraction 66% +/- 8%) and 15 (53 +/- 11 years) healthy control subjects (ejection fraction 61% +/- 5%) were included in the analysis. Regional function was studied in four parallel equidistant short-axis cross sections from base to apex of the reconstructed left ventricle. In 15 degree intervals, 24 wall thickness measurements in each cross section were made at end-diastole and end-systole after endocardial and epicardial border tracing. A total of 192 measurements were obtained in each patient, and absolute wall thickening and fractional thickening were calculated. Absolute and fractional wall thickening showed a significant inverse relation to end-diastolic wall thickness in all heart conditions (r = 0.71, p < 0.0001). Regions of normal wall thickness in diseased patients were not hyperdynamic when compared with normal control subjects. Significant impairment in fractional thickening at identical end-diastolic thickness was observed in the septum compared with the lateral free wall in both hypertrophic cardiomyopathy and hypertensive heart disease. Thus regional systolic function is inversely related to end-diastolic wall thickness. The decrease in regional systolic function with increasing LV hypertrophy was similar in idiopathic and hypertensive cardiomyopathy. In both types of hypertrophy, significant differences in systolic function were observed in septal and lateral wall segments of similar wall thickness. This indicates that factors other than end-diastolic wall thickness influence myocardial thickening in patients with hypertrophy and preserved global function.
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PMID:Evaluation of regional systolic function in hypertrophic cardiomyopathy and hypertensive heart disease: a three-dimensional echocardiographic study. 971 89

Hypertrophic cardiomyopathy is the most common cause of sudden death in young individuals who are otherwise healthy. Risk of sudden death is highest in patients who are between 14 and 35 years old. Several mechanisms are involved in sudden death: ventricular arrhythmias, supraventricular arrhythmias leading to cardiac collapse, bradycardias and severe ischemia. Many studies have analyzed how to identify high risk patients. The factors that best identify high risk patients are: previous history of sudden death or syncope, induction in adults of sustained ventricular arrhythmias, the presence of non-sustained ventricular tachycardia in symptomatic patients, the presence of ischemia associated with hypotension in children, the presence of mutations in the beta-myosin heavy chain together with a family history of sudden death and a poor left ventricular ejection fraction. Risk stratification should be done on an individualized basis. In those patients in whom a high risk for sudden arrhythmic death is suspected, the only current effective treatment is the implantable defibrillator.
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PMID:[Sudden death in hypertrophic myocardiopathy]. 992 51


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