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)

The main blood flow velocity patterns in the LVOT and RVOT were recorded by pulsed Doppler echocardiography in 28 normal healthy cases, in two athletes, and in 85 patients with atrial septal defects, pulmonary regurgitation, tetralogy of Fallot, aortic regurgitation, mitral stenosis, aortic stenosis, mitral regurgitation, hypertrophic cardiomyopathy, ischemic heart disease, and pulmonary hypertension. Blood flow velocities were displayed using a graphic system to form a real time sonogram, using Fast Fourier Transformation. In the normal group, the blood flow velocity was 1.69 KHz in LVOT, and 1.71 KHz in RVOT. In AR and T/F but not MS, there was high blood flow velocity in the LVOT, and the peak of blood flow velocity was shifted to mid-to late systole. In ASD and VSD with a L-R shunt, high blood flow velocity occurred in the RVOT, and the peak velocity shifted to early systole. Pulmonary hypertension occasionally produced a W- or V-shaped curve. In normal subjects, a small "a" wave could be detected in the LVOT recording. The "a" wave began at point B on the AML tracer of the M-mode echocardiography, reached maximum velocity at point C, and returned to zero (baseline) at point C'. The "a" wave was coincident with the R wave of the ECG, and with the Ia of the phonocardiogram (PCG). The normal velocity of the "a" wave was 602 Hz, and the a/H ratio was 0.36. In cases of HCM and IHD, the "a" wave velocity and the a/H ratio correlated with the end diastolic pressure and the peak dP/dT. These data suggest that the Doppler blood flow patterns in the LVOT and RVOT can indicate volume overload in the right and left ventricles, and that the "a" wave velocity and a/H ratio can provide new information concerning cardiac performance.
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PMID:Main systolic blood flow patterns in the left and right ventricular outflow tracts determined by Doppler echocardiography. 404 Jul 20

Age, sex and cause-specific mortality rates in 1982-86 for eight municipalities in the Tel Aviv region were compared to comparable rates of a reference population--the 1984 Jewish population of Israel. Residents of Or Yehuda, Tel Aviv, Holon and Bat Yam had an elevated risk of dying. Of particular interest is the elevated risk among adult residents of the Tel Aviv municipality. Males and females aged 30-44 had excess mortality from heart disease and external causes of death, and males aged 45-64 from ischemic heart disease and external causes. Tel Aviv females aged 30-44 also had excess mortality from cerebrovascular disease and females aged 45-64 from malignancy. High mortality rates in these age groups contribute considerably to years of life lost, and it is suggested that local health service or governmental action should be taken to investigate and reduce the disparities. Small area analysis, as shown here, may provide considerable information for monitoring community health.
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PMID:Variation in mortality rates in Tel Aviv region municipalities. 808 86

Stroke during sleep is an unexplored area of vascular neurology and its pathogenesis; clinical significance and prevention still remain uncertain. The aim of our study was to determine the epidemiological and clinical patterns of ischemic stroke occurring during sleep. Consecutive patients (n = 1822) with acute ischemic stroke recorded in the Tel Aviv Stroke Register were studied. Stroke during sleep was determined whenever focal neurological deficit was verified to have occurred while the patient had been asleep. The comparisons between patients with stroke during sleep and while awake were performed using the t test with Bonferroni correction and the chi(2) test for age, sex, vascular risk factors (i.e. ischemic heart disease, myocardial infarction, atrial fibrillation, arterial hypertension, hyperlipidemia, diabetes mellitus, peripheral vascular disease, smoking), vascular distribution (carotid versus vertebrobasilar) and severity of stroke (mild, moderate or severe). Data regarding the onset of stroke (during sleep or while awake) were available for 1,671 patients. A minority of strokes occurred during sleep (n = 311, 18.6%), and stroke during sleep was severer (chi(2) = 11.9, p < 0.002). No significant differences were found in terms of age, sex and vascular distribution between the two groups. None of the vascular risk factors was found to be more frequent in stroke during sleep. Strokes occurring during sleep were found to be severer than those with onset while awake. However, no specific clinical patterns of risk factor profiles could be identified in these patients. Hemodynamic factors may play an important role in the occurrence of stroke during sleep, and this issue should be further investigated.
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PMID:Stroke during sleep: epidemiological and clinical features. 1054 88

It is now accepted that the incidence of ischaemic stroke is significantly increased in the morning. Any attempts to prevent its occurrence must be based on determining the mechanisms, special risk factors and appropriate protective measures needed during this vulnerable period. We studied the epidemiological features of morning stroke and reviewed the records of 2312 consecutive patients recorded prospectively in the Tel Aviv Stroke Register. Information about time of stroke onset was obtained from the patient, family members or other observers. The study parameters of age, sex, vascular distribution (carotid versus vertebrobasilar), ischaemic heart disease, myocardial infarction, diabetes mellitus, arterial hypertension, smoking, hyperlipidaemia, stroke severity and recurrence were compared between patients with morning stroke and those with stroke occurring at other times. In 599 patients (34%) stroke occurred between 06:00 and 10:00 h. No evaluated parameter was found to be statistically different among the morning stroke patients compared with stroke occurring at other times (P < 0.2). Patients with arterial hypertension and ischaemic heart disease and male patients had a greater likelihood of stroke occurrence between 22:00 and 02:00 h (P < 0.05). Our data suggest that none of the common vascular risk factors could explain the morning peak of stroke occurrence. The next step in the quest for understanding the phenomenon of circadian variation is to identify other physiological factors and the effects of pharmacological agents in morning stroke protection.
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PMID:Are there any unique epidemiological and vascular risk factors for ischaemic strokes that occur in the morning hours? 1080 38

A 77-year-old man was diagnosed as having essential thrombocythemia (ET) in 1994. He had been treated with hydroxyurea (HU) for six years, and 9 years after the diagnosis of ET, he then developed acute myelomonocytic leukemia (AMMoL) following myelodysplastic syndrome (MDS). Since he suffered from ischemic heart disease, we chose the ara-C+VP-16 therapy. Two courses of the ara-C+VP-16 therapy resulted in partial remission in the bone marrow and a prolonged hematological response. This case seemed rare, since in previous reports, prognosis of ET patients developing MDS and AML was very poor and most of the patients expired within six months.
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PMID:[Successful treatment of acute myelomonocytic leukemia developed from essential thrombocythemia with cytarabine plus etoposide]. 1560 90

The main reason for myocardial dysfunction is chronical myocardial ischemia. Recently we could show, that NCAM (CD56), a neural cell adhesion molecule and member of the immunoglobuline superfamily, and the transcription factor AML1 (RUNX1) are overexpressed in chronic ischemic human heart failure compaired to normal hearts. Here we demonstrate, that the overexpression of NCAM (CD56) is specific for ischemic damage as compaired to other heart diseases including congestive cardiomyopathy, hypertrophic obstrutive cardiomyopathy, myocarditis and sarcoidosis. Concerning the transcriptional regulation of NCAM (CD56) by AML1 (RUNX1) we isolated 3 novel isoforms of AML 1 (RUNX1) with different transactivating function, that might be a regulatory element of the NCAM (CD56) overexpression in chronical myocardial ischemia.
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PMID:[The overexpression of NCAM (CD56) in human hearts is specific for ischemic damage]. 1689 59