Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0151744 (myocardial ischemia)
 31,282 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We performed signal-averaged electrocardiography and 24-h ambulatory electrocardiographic monitoring in 53 patients with myotonic dystrophy to determine the incidence and clinical significance of ventricular late potentials. Patients were followed up for a mean period of 31 +/- 17 months (range 11-68 months). At entry, none of the patients had bundle branch block on 12-lead electrocardiogram and none had wall motion abnormalities on routine echocardiogram. Also, no patient had history of syncope or clinical evidence of ischemic heart disease or a documented sustained ventricular tachycardia. A group of 47 healthy subjects matched for age and sex also underwent signal-averaged electrocardiography for comparison with the patient group. Late potentials were diagnosed in the presence of at least two of the following measures: duration of the filtered QRS > 114 ms, root-mean-square voltage of the terminal 40 ms of the filtered QRS < 20 microV, and duration of the low-amplitude (< 40 microV) signals of terminal filtered QRS > 38 ms. Late potentials were more frequent in patients than in controls: 18 of the 53 patients (34%) showed late potentials compared with four of the 47 controls (8.5%) (P < 0.01). In 45 patients (85%) no ventricular ectopy (40 cases) or infrequent premature ventricular complexes (five cases) were detected on Holter monitoring. Complex ventricular arrhythmias were traced in the remaining eight patients. These were six of the 18 patients with, and two of the 45 patients without late potentials (33% vs. 6%, respectively; P < 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Signal-averaged electrocardiography in myotonic dystrophy. 755 65

Two women with myotonic dystrophy underwent dipyridamole thallium-201 (201Tl) myocardial perfusion imaging, after which one patient developed flat T waves in lead I and aV(L), and inverted T waves in leads V(2-6). The other patient developed a nonspecific intraventricular block that progressed to complete left bundle branch block and was associated with chest discomfort. Reversible scintigraphic defects were observed in both women. Although there was evidence that suggested myocardial ischemia on the ECG changes and 201Tl scintigraphic findings, coronary angiography demonstrated no significant stenoses in either patient. These findings suggest that microvascular dysfunction may lead to myocardial ischemia and conduction disturbances in patients with myotonic dystrophy.
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PMID:Microvascular ischemia in patients with myotonic dystrophy. 1098 60

The aim of this study was to assess the changes in hemodynamic function and myocardial perfusion of the left ventricle occurring in patients with type 1 diabetes mellitus (DM1) 47-49 months after the first assessment. We have studied 20 asymptomatic patients, five females and 15 males, aged 22-46 y. The patients were under intensive insulin treatment and had normal electrocardiogram (ECG) at rest. In all patients gated single photon emission tomography (GSPET) was performed at rest and after exercise (examination I). After 47-49 months this test was repeated (examination II). GSPET was performed 60 min after the intravenous injection of 740 MBq of technetium-99m 2-methoxy-isobutyl-isonitrile ((99m)Tc-MIBI), using a dual-headed gamma-camera. Left ventricular ejection fraction (LVEF), end diastolic volume (EDV) and end systolic volume (ESV) were calculated using quantitative GSPET (QGS). The intensity of perfusion defects was also evaluated based on a four degree QGS scale. Our results were as follows: a) In examination I, performed at rest: LVEF was 56.1%+/-7.5%, EDV 96.9+/-25.8 ml and ESV 42.6+/-16.3 ml. b) In examination I at stress: LVEF was 57.2%+/-7.5%, EDV 94.1+/-24.0 ml and ESV 40.5+/-15.5. c) In examination II performed at rest: LVEF was 58.1%+/-6.5%, EDV 112.1+/-26.1 ml and ESV 46.6+/-14.9 ml and d) In examination II at stress: LVEF 57.8%+/-5.6%, EDV 107.9+/-27.4 ml and ESV 44.9+/-14.4 ml. Significant differences were found between examinations I and II, regarding: a) EDV at rest (P<0.001) and at stress (P<0.001) and b) ESV at rest (P<0.05) and at stress (P<0.005). Correlation analysis revealed significant correlation between LVEF at rest and at stress both in examination I (r=0.83; P<0.001) and also in examination II (r=-0.897; P<0.001). Intensity of myocardial perfusion defects in examination I at rest and at stress was: 1.68+/-0.5 and 2.2+/-0.6 degrees respectively. Intensity of myocardial perfusion defects in examination II at rest and at stress was: 1.75+/-0.4 and 2.2+/-0.5 respectively. No significant differences in the intensity of these perfusion defects were found. EDV both at rest and at stress was significantly higher in examination II as compared with the examination I study. Similar, but less pronounced changes of ESV were found. This study confirms other authors' observations on LV, EDV and LV, ESV and also that the percentage of asymptomatic DM1 patients having silent myocardial ischemia is high as was in all our patients. Nevertheless, in the current literature, we were unable to find a study similar to the present one, comparing basal and after four years LV functional GSPET data, in asymptomatic DM1 patients. In conclusion, myocardial perfusion GSPET was useful as a screening test in DM1 patients in showing four years after the basal study, prodromal signs of cardiovascular disease, especially increase of left ventricular volumes and silent myocardial ischemia, in these patients. Our research on the above protocol is being continued.
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PMID:Evaluation of the left ventricular hemodynamic function and myocardial perfusion by gated single photon emission tomography, in patients with type 1 diabetes mellitus; prodromal signs of cardiovascular disease after four years. 1689 11

Myotonic dystrophy type 1 (MD1) is an autosomal dominant disorder characterized by myotonia, progressive muscular weakness, cataract, and cardiac involvement. Cardiac involvement is common and includes conduction system abnormalities, supraventricular and ventricular arrhythmias, and less frequently, myocardial dysfunction and ischemic heart disease. A 54-year-old woman with a previous diagnosis of MD1 was admitted with palpitation, blood pressure of 157/118 mmHg, and a heart rate of 220 beats/min. Electrocardiography (ECG) showed ventricular tachycardia. Within minutes, hemodynamic collapse developed and electrical cardioversion was performed. Immediately following cardioversion, ECG showed atrial fibrillation, a slightly prolonged QT interval, and intraventricular conduction delay. After intravenous infusion of amiodarone, the rhythm converted to sinus. Transthoracic echocardiography showed significantly depressed left ventricular function, an ejection fraction of 25%, and normal coronary arteries. During electrophysiological study, atrium-His interval and His-ventricle interval were 120 msec was 54 msec, respectively, and monomorphic ventricular flutter was induced. An implantable cardioverter-defibrillator was placed. She was discharged in sinus rhythm.
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PMID:A case of myotonic dystrophy presenting with ventricular tachycardia and atrial fibrillation. 1987 8

Myotonic dystrophy (MD) is a neuromuscular disorder of autosomal dominant inheritance, which is categorized by 2 main sub-types: type 1 (MD1) and type 2 (MD2). This disease is characterized by myotonia and various multisytemic complications, most commonly of the cardiac, endocrine, and central nervous systems. In addition, cardiac abnormalities contribute to a significant morbidity and mortality in these patients. The cardiac abnormalities common to MD1 are conduction defects, such as first-degree atrioventricular block, arrhythmias, and other less common manifestations such as heart failure, ischemic heart disease, and mitral valve prolapse. Although these cardiac manifestations are also common in MD2, another complication that has been linked to MD2 is cardiomyopathy. Further study needs to be performed to better understand the pathology and management of these cardiac disorders associated with MD.
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PMID:Myotonic dystrophies and the heart. 2214 78